2021 Conference New Targets, New Approaches September 22-25, 2021 - Loews Ventana Canyon Resort
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Lupus 21st Century
2021 Conference
New Targets, New Approaches
September 22-25, 2021
Loews Ventana Canyon Resort
Tucson, AZ, U.S.A.
Lupus 21st Century
Conference
ABOUT LUPUS 21ST CENTURY
Mission Statement
Interactive meeting, integrating North American, South American, Caribbean,
and European scientific experts, to stimulate discussion, identify problems,
and promote collaborative solutions and strategies to improve treatments and
outcomes for lupus patients
Objectives
Enhance awareness of expertise across the basic to applied clinical sci-
ence spectrums as they relate to ongoing research advances in lupus.
Review most recent updates in basic and clinical sciences and how they
could apply to the management of patients with lupus.
Create an environment for small group discussion to enhance the
productivity and transfer of know ledge of research in lupus.
Support aspiring basic and clinical scientists and start networking at
the beginning of their career.
Foster discussion between researchers and patients to facilitate the
involvement of patient needs into the research agenda.
Lupus 21st
1 Century
LUPUS 21ST CENTURY AWARDS
Randy T Fischer Award for Excellence in Basic Research
Awarded in recognition of outstanding discoveries pertinent to the fundamental biology of lupus.
Halsted R. Holman Award for Excellence in Clinical Research
Awarded in recognition of an outstanding achievement that bridges new discoveries in lupus care with an
understanding of what works, for whom, at what cost, and the practical barriers to their application.
Lawren H. Daltroy Award for Excellence in Health Communication
Awarded in recognition of work that bridges the gap between words and understanding in provider-patient
communications.
Charles L. Christian Award for a Significant Advance in Understanding Lupus
Awarded to a mid-career investigator who has made a significant advance in understanding the pathogenesis
impact or treatment of lupus
Joachim Kalden Award for Excellence in Clinical Immunology
This award is given in respectful remembrance of Professor Joachim Kalden, a pioneering giant in clinical
immunology, to a scientist who has made meaningful contributions in the application of principles of
clinical immunology to the better understanding of systemic lupus erythematosus
The Living Better with Lupus Award
Awarded to a lupus patient who has made significant sacrifices of time and resources in raising lupus
awareness on a community, state, and national level.
Lupus 21st Century Steering Committee Members Event Organizers
Joy Buie (Charleston, SC, United States) Claire Dykas (Charlottesville, VA, United States)
Karen Costenbader (Boston, MA, United States) Julie Parrot (Québec, QC, Canada)
Peggy Crow (New York, NY, United States) Kate Vega (Tucson, AZ, United States)
Maria Dall’Era (San Francisco, CA, United States) Brooke Williams (Charlottesville, VA,
John Esdaile (Vancouver, BC, Canada) United States)
Paul R. Fortin (Québec, QC, Canada)
Matthew Liang (Boston, MA, United States)
Peter Lipsky (Charlottesville, VA, United States)
Timothy Niewold (New York, NY, United States)
Tyresa Sellers (Cambria Heights, NY, United States)
Anne Stevens (Philadelphia, PA, United States)
Lupus 21st
Century 2
PROGRAM AT A GLANCE
All sessions will take place in Mountain Time.
Wednesday, September 22, 2021
6:00 PM – 8:00 PM Welcome Reception
Thursday, September 23, 2021
Time Details
7:00 AM – 8:00 AM Breakfast
8:00 AM – 8:15 AM Welcome
8:15 AM – 9:45 AM Mechanisms of Brain Injury in Inflammatory Diseases
9:45 AM – 1 0:00 AM Break
10:00 AM – 12:00 PM Patient Session: New Developments and Patient Year in Review
Concurrent Sessions I
• Cutaneous Lupus
• Lupus Nephritis
• T Cells
• PROs
12:00 PM – 12:30 PM Lunch
12:30 PM – 2:00 PM Workshops
2:00 PM – 4:00 PM The Impact of Ancestry on SLE Phenotypes
4:00 PM – 6:00 PM Poster Discussions
6:00 PM – 8:30 PM Dinner
Friday, September 24, 2021
Time Details
7:00 AM – 8:00 AM Breakfast
8:00 AM – 10:30 AM The Macrophage as a Jack of All Trades:
Development, Homeostasis, Damage and Repair
10:30 AM – 10:45 AM Break
10:45 AM – 12:00 PM How Do We Learn What Works (and What Harms)
When No Randomized Trials Exist?
12:00 PM – 12:30 PM Lunch
12:30 PM – 2:00 PM Workshops
2:15 PM – 4:30 PM Lupus Nephritis
4:30 PM – 6:30 PM Poster Discussions
6:30 PM – 9:00 PM Dinner
Saturday, September 25, 2021
Time Details
7:00 AM – 8:00 AM Breakfast
8:00 AM – 10:30 AM The Immunology of Nucleic Acids in SLE
10:30 AM – 10:45 AM Break
10:45 AM – 12:45 PM Patient Session: Covid and Lupus
Concurrent Sessions II
• Innate Immunity and Vascular Complications
• B Cells and Autoimmunity
• Genetics and Genomics
• Lupus-Targeted Therapeutics
12:45 PM – 3:00 PM Lunch & Discussions
3:00 PM – 4:00 PM Keynote Presentations
• Sars-Cov-2 in Patients with Autoimmune Disease: A Review
• Overview of Antibodies in Covid-19
4:00 PM – 4:45 PM Awards Ceremony
4:45 PM – 6:00 PM Independent Discussions
6:00 PM – 9:00 PM Dinner
Lupus 21st
3 Century
SCIENTIFIC PROGRAM
WEDNESDAY, 22 SEPTEMBER 2021
6:00 PM – 8:00 PM Welcome Reception Cascade Terrace
THURSDAY, 23 SEPTEMBER 2021
7:00 AM – 8:00 AM Breakfast Cascade Terrace
8:00 AM – 8:15 AM Welcome Ballroom BC
Mechanisms of Brain Injury in Inflammatory Diseases
Chair: Peggy Crow
o Introduction to CNS Lupus – John Hanly
8:15 AM – 9:45 AM Ballroom BC
o Type I Interferon in CNS Pathology – Wei Cao
o Mechanisms of CNS Disease in Lupus – Michael Carroll
o Nucleic Acid Regulation in Neuronal Cells – Hachung Chung
9:45 AM – 10:00 AM Break Foyer-Grand Ballroom
Patient Session: New Developments and Patient Year in Review Coronado Room
Concurrent Sessions I
Cutaneous Lupus
Salon E
Co-Chairs: Michelle Kahlenberg and Theresa Lu
10:00 AM – 12:00 PM Lupus Nephritis
Salon C
Co-Chairs: Marcus Clark and Gabriel Contreras
T Cells
Salon F
Co-Chairs: Deepak Rao and Jeremy Tilstra
PROs
Salon B
Co-Chairs: John Esdaile and Meenakshi Jolly
12:00 PM – 12:30 PM Lunch Foyer-Ballroom
Workshops
The Genetic and Environmental Origins of SLE
12:30 PM – 2:00 PM Chair: John Harley
Can a reliable lupus study still be done?
Chair: Daniel Wallace
The Impact of Ancestry on SLE Phenotypes
Chair: Amrie Grammer
o Introduction – Carl Langefeld
o Understanding the Influence of Ancestry on SLE Disease
Mechanisms – Katherine Owen
2:00 PM – 4:00 PM Ballroom BC
o Ancestral Differences in Cytokine Regulation in Lupus –
Timothy Niewold
o APOL1-Associated Nephropathy: At the Bedside… Far
Beyond the Bench – Barry Freedman
o Integrating Genetic and Social Factors to Understand
Health Disparities in Lupus – Paula Ramos
4:00 PM – 6:00 PM Poster Discussions Foyer-Ballroom
6:00 PM – 8:30 PM Dinner Upper Terrace
Lupus 21st
Century 4
FRIDAY, 24 SEPTEMBER 2021
7:00 AM – 8:00 AM Breakfast Cascade Terrace
The Macrophage as a Jack of All Trades:
Development, Homeostasis, Damage and Repair
Chair: Harris Perlman
INTRODUCTION – Anne Davidson
DEVELOPMENT AND HOMEOSTASIS
o Macrophage Development – Florent Ginhoux
MACROPHAGES AND DISEASE
8:00 AM – 10:30 AM A. Inflammation and Metabolism Ballroom BC
o Renal Myeloid Cells, Recruitment, and Function –
Laura Denby
o Beyond Pruning and Inflammation: How Microglia
Participate in Neuronal Activity – Anne Schaefer
B. Macrophages and Repair
o Macrophage Metabolism and Atherosclerosis and Repair –
Kathryn Moore
o Macrophages in Fibrosis and Repair – Scott Budinger
SUMMARY AND QUESTIONS
10:30 AM – 10:45 AM Break Foyer-Grand Ballroom
How Do We Learn What Works (and What Harms)
When No Randomized Trials Exist?
Chair: John Esdaile
o Introduction – Karen Costenbader
10:45 AM – 12:00 PM Ballroom BC
o Observational Studies in Rheumatic Diseases: Avoidable
Pitfalls – Samy Suissa
o Using Observational Data to Emulate Hypothetical
Randomized Trials – Miguel Hernan
12:00 PM – 12:30 PM Lunch Foyer-Ballroom
Workshops
12:30 PM – 2:15 PM Advancing Childhood Lupus: Leveraging Existing Registries and Ongoing
Clinical Trials for Translational Studies
Chair: Hermine Brunner
2:15 PM – 4:30 PM Lupus Nephritis
Chair: Maria Dall’Era
o Introduction – Betty Diamond
o Spatial Relationship of Cells in Lupus Nephritis –
Paul Hoover
o Kidney Profiling of Lupus Nephritis Patients in AMP: Ballroom BC
An Update – Arnon Arazi
o Impact of Vascular Injury Derived Humoral Responses in
Lupus Nephritis Development – Mélanie Dieudé
o Learning from Repeat Biopsy in LN – Brad Rovin
o Combination Therapy of LN – Hans-Joachim Anders
4:30 PM – 6:30 PM Poster Discussions Foyer-Ballroom
6:30 PM – 9:00 PM Dinner Ballroom BC
Lupus 21st
5 Century
SATURDAY, 25 SEPTEMBER 2021
7:00 AM – 8:00 AM Breakfast Cascade Terrace
The Immunology of Nucleic Acids in SLE
Chair: Peter E Lipsky
o Introduction – David Pisetsky
o Molecular Properties of Extracellular DNA in SLE and Other
Conditions – Dennis Lo
o Extrachromosomal Circles of DNA in Normal Mammalian
Tissues – Anindya Dutta
8:00 AM – 10:30 AM Ballroom BC
o Left-Handed DNAs and RNAs That Regulate Inflammation –
Alan Herbert
o The Role of cGAS-STING Signaling in Immune and
Autoimmune Responses – James Chen
o The Detection of DNA Damage and Replication Stress as
Danger Signal in Skin Cells – Leonie Unterholzner
o DNA Sensing by AIM2 – Kate Fitzgerald
10:30 AM – 10:45 AM Break Foyer-Grand Ballroom
Patient Session: Covid and Lupus Coronado Room
Concurrent Session II
Innate Immunity and Vascular Complications
Salon E
Co-Chairs: Keith Elkon and Westley Reeves
B Cells and Autoimmunity
10:45 AM – 12:45 PM Salon E
Co-Chairs: Keith Elkon and Westley Reeves
Genetics and Genomics
Co-Chairs: Andrea Daamen, Patrick Gaffney, Mikhail Olferiev, and Salon F
Amr Sawalha
Lupus-Targeted Therapeutics
Salon C
Co-Chairs: Cynthia Aranow and Anca Askanase
12:45 PM – 3:00 PM Lunch & Discussions Foyer-Ballroom
Keynote Presentations
Co-chairs : Paul Fortin and Anne Stevens
3:00 PM – 4:00 PM o Sars-Cov-2 in Patients with Autoimmune Disease: Ballroom BC
A Review – Kevin Winthrop
o Overview of Antibodies in Covid-19 – PJ Utz
4:00 PM – 4:45 PM Awards Ceremony Ballroom BC
4:45 PM – 6:00 PM Independent Discussions
6:00 PM – 9:00 PM Dinner Coyote Corral
Lupus 21st
Century 6
CONCISE ABSTRACT SUMMARIES
All abstracts will be published in Lupus Science & Medicine. depression, psychosis) and psychological (e.g. cognitive impairment,
anxiety) symptoms during the course of their illness. Many of these
nervous system events can also occur for reasons unrelated to lupus;
in fact only one third to a half are felt to be due directly to SLE. We
100 - BRAIN INJURY IN SLE wished to know which SLE patients were more likely to develop these
events and when they occurred which patients were more likely to
have the symptoms resolve. To answer these questions we followed
1,827 lupus patients around the world over an average of seven-
Abstract Number: 101 and-half years and carefully documented all of their nervous system
events, regardless of the cause. We then decided which events were
Increased Blood Brain Barrier Permeability Associates with likely due to SLE or to other causes. Finally, using information on
Increased Hippocampal Glucose Metabolism In SLE patients’ demographics (e.g., age, sex, race/ethnicity and education),
Meggan Mackay features of SLE (e.g. SLE disease activity, organ damage and lupus
medications) and laboratory tests (e.g. lupus autoantibodies) we
Up to 80% of lupus patients experience problems with cognition,
identified which factors were helpful in predicting the onset and
meaning problems with memory and concentration. Studies have
resolution of NP events due to SLE and NP events due to non-SLE
shown that some of the cognitive problems in lupus are caused
causes.
by inflammatory mechanisms from lupus itself. However, under
normal circumstances the brain is protected by a blood brain barrier
that prevents inflammatory molecules, such as autoantibodies,
from accessing the brain. In this study, special brain imaging, Abstract Number: 104
DCE-MRI, was used to measure blood brain barrier permeability
in lupus patients and healthy individuals. We found that there Distinct Spatial Profile of Inflammatory Gene Expression in the
was abnormally increased blood brain barrier permeability in the Brain of a Mouse Model of Neuropsychiatric Lupus
hippocampus of lupus patients. The area of increased blood brain Michael Carroll
barrier permeability in the hippocampus overlapped with a similar
area of abnormally increased brain metabolism in the hippocampus Lupus patients frequently develop neurological symptoms;
in the same lupus patients. These findings are important because however, the underlying basis for the symptoms is not understood.
the hippocampus is the center for memory in the brain. Using a mouse model of lupus, we find that they also have behavior
changes and the mice develop distinct patches of inflammation
among various regions of the brain. These results provide novel bio-
markers in a mouse model to test new therapeutic approaches for
Abstract Number: 102 treatment of NPSLE.
Potential Biomarkers of Cognitive Impairment in the Context of
Childhood-Onset Systemic Lupus Erythematosus
Andrea M Knight
200 - CUTANEOUS SLE
Cognitive changes are thought to occur in as many as 60% of
patients with childhood-onset lupus. Patients with cognitive
changes have trouble with attention, focus, memory, and making
Abstract Number: 201
decisions. These changes can have a negative impact on school
performance and social interaction and exert long-term effects. Type I Interferon Modulates Langerhans Cell ADAM17 in Lupus
Yet, we face significant challenges in diagnosing and treating to Contribute to Photosensitivity
young patients with lupus and cognitive involvement. We do not Theresa T. Lu
understand why the cognitive changes occur. We do not have
Anifrolumab has good effects for lupus skin disease but the
accurate tools for diagnosis. We do not have precise treatment.
mechanisms by which type I interferon contributes needs to be more
These challenges can lead to delays in diagnosis and treatment, as
clearly understood. Photosensitivity is an underlying factor for lupus
well as under-treatment or over-treatment of young patients with
skin disease, and here we show that type I interferon contributes
lupus. In this study, we used advanced magnetic resonance imaging
to photosensitivity by causing dysfunction of Langerhans cells, a
(MRI) techniques to identify brain changes associated with changes
skin immune cell that normally protects the skin from sun-induced
in cognitive function. We also looked for other features of lupus
injury. Our results have implications for better understanding how
that may be associated with changes in cognitive function. In our
anifrolumab works in lupus skin disease and delineating additional
sample of 24 children with lupus, we found that 42% had cognitive
potential therapeutic targets.
impairment. This impairment was associated with changes in brain
structure in certain regions, and with higher levels of inflammation
and older age. The results of this study help us to better understand
how cognitive changes occur in children with lupus, and who is most Abstract Number: 202
at risk. We will continue this work to look at larger patient samples
over time, and also compare our results to healthy children. We hope Causes of Death Among Populations with Systemic Lupus
that this will ultimately improve the diagnosis and treatment of Erythematosus by Sex, Race and Ethnicity
cognitive involvement for patients with lupus. Milena Gianfrancesco
Minority populations with lupus are at higher risk of developing
disease and have more severe outcomes, including death. However,
Abstract Number: 103 whether specific causes of death differ by race and ethnicity
has largely been unexplored, particularly for Asian and Hispanic
Neuropsychiatric Events in Systemic Lupus Erythematosus: individuals. This study identified all lupus cases in San Francisco
Predictors of Occurrence county during 2007-2009, and then merged death certificate
John Hanly information up to 10 years later to identify specific causes of death.
There were 135 deaths identified within a group of 809 individuals
Patients with systemic lupus erythematosus (SLE) may experience
with lupus. The top underlying cause of death overall (33%) and
a variety of neurological (e.g. stroke, seizures), psychiatric (e.g.
Lupus 21st
7 Century
across all racial and ethnic groups was cardiovascular disease (CVD). 300 - TRANSCRIPTOMICS
In comparison to the general population of San Francisco county,
CVD as the underlying cause of death was over three times higher
among individuals with lupus. CVD deaths for those with lupus
also were nearly three times higher for Black, approximately four Abstract Number: 301
times higher for Asian, and over six times higher for Hispanic/Latino
individuals. Our results show that CVD is the leading underlying Differentially Expressed Transcripts Associated with Lupus Risk
cause of death among lupus patients across various racial and Loci Identify Pathogenic Disease Pathways
ethnic groups, and that Asian and Hispanic/Latino lupus patients Mikhail Olferiev
experience a disproportionate burden of death associated with CVD
compared to the general population. Combining information from analysis of genes expressed by blood
cells with published information about regions of the human
genome associated with risk of developing lupus, we have identified
Abstract Number: 203 groups of genes that track together and point to important immune
mechanisms that contribute to disease. We have compared data
from males and females with lupus, allowing identification of those
Non-Lesional and Lesional Lupus Skin Share Inflammatory
molecular mechanisms most relevant to development of lupus in
Phenotypes that Drive Activation of CD16+ DCs
men.
J. Michelle Kahlenberg
Cutaneous lupus erythematosus (CLE) is a common manifestation of
systemic lupus and lesions can be refractory to current therapies. This Abstract Number: 302
study used single cell RNA sequencing and spatial transcriptomics to
uncover a new understanding of the cell populations in both lesional Transcriptomic Analysis Reveals a Critical Regulatory Role For
and non-lesional lupus skin in order to advance our ability to treat CD8 T Cells in a Mouse Model of Systemic Lupus Erythematosus
CLE. Interestingly, the skin of lupus patients showed inflammatory
cells with or without lesions present, and the recruitment of a Andrea R. Daamen
subpopulation of dendritic cells into lupus skin demonstrated that Systemic lupus erythematosus (lupus) is a complex autoimmune
the cells are educated by the skin itself so that the cells are more disease characterized by the production of antibodies that target a
inflammatory when they are in the skin than when they are in the person’s own tissues, leading to systemic inflammation.
blood. This suggests that the skin itself contributes to the risk of Mice that develop spontaneous lupus-like disease have been
inflammation in patients prone to CLE. important tools for investigating the immune response in lupus
patients and testing potential treatments before introducing them
to the clinic. To obtain a snapshot of the immune response in lupus,
Abstract Number: 204 we have developed a number of tools to identify specific immune
cell types and pathways that are abnormal in lupus patients and
The Role of Neutrophils in the Clinical Severity have adapted these tools for analysis of mouse datasets.
of Lupus Nephritis Patients with Concurrent Skin
Disease The BXSB.Yaa mouse develops a spontaneous lupus-like disease
that is accelerated in the absence of CD8 T cells (BXSB.DKO mice).
Sladjana Skopelja-Gardner CD8 T cells are an immune cell population that has not been well
Exposure to sunlight worsens disease symptoms in most lupus characterized in lupus. For some patients, CD8 T cells appear
patients, including kidney disease. Our recent findings suggested to contribute to worse disease, whereas in others, they may be
that the most abundant white blood cells in blood, neutrophils, may protective. Therefore, we have used gene expression analysis of Yaa
play an important role in the worsening of kidney disease because and DKO mice to clarify the role of CD8 T cells in lupus. We found that
of skin inflammation. In this study, we showed that lupus nephritis in the absence of CD8 T cells, DKO mice had increased expression of
patients who have a skin rash at the time of kidney disease flare have genes associated with an immune cell similar to an M2 macrophage
more neutrophils in their blood. High numbers of neutrophils in with high capacity for engulfment and tissue repair. DKO mice also
these patients associated with worse kidney function. Interestingly, had increased expression of some pro-inflammatory genes and
lupus nephritis patients who had high neutrophil levels in the decreased expression of important anti-inflammatory genes that
presence of a skin rash also had increased presence of a specific could contribute to disease pathology. Overall, our results suggest
antibody type (IgA) in their kidneys. Given previous knowledge that CD8 T cells may play a protective function in BXSB.Yaa mice
that IgA can potentiate neutrophil inflammatory functions, we are through regulating the outgrowth of M2-like macrophages. This
intrigued by this link and its possible implications for how skin injury work could have critical implications for lupus patients that have
can worsen kidney disease in lupus. decreased function of these regulatory CD8 T cells.
Abstract Number: 303
Abstract Number: 205
A Stepwise Transcriptomic Analysis Using Gene Modules
Lymphatic Dysfunction in Lupus Photosensitivity and Immune Cell Signatures to Stratify Systemic Lupus
William G Ambler Erythematosus Patients and Identify Potential Treatment
The skin communicates with the body and immune system through Targets
lymphatics. Small lymphatic vessels carry cells, molecules, and fluid Jozsef Karman
from skin to lymph nodes where immune cells reside. Patients with SLE is a highly heterogeneous disease. We have taken advantage
lupus frequently are photosensitive and can develop skin rashes and of the large amount of gene expression data collected over the last
systemic disease flares after sun exposure. In animal models, poor decade to devise methods to better understand this heterogeneity
lymphatic drainage worsens photosensitivity, thus we hypothesized and understand differences in gene expression in between subsets
that lymphatic dysfunction could contribute to photosensitivity in of SLE patients. We hope that these methods and the results they
lupus. We found that photosensitive lupus mice have poor lymphatic generated will lead to better understanding of disease mechanisms
drainage. Improving lymphatic drainage using several techniques, in subsets of SLE patients and eventually lead to more tailored
including simple manual drainage, improves photosensitivity disease modifying approaches to individual SLE patients.
and may alter the systemic immune response. Understanding
mechanisms of lymphatic dysfunction and how it contributes to
photosensitivity in lupus could give light to novel therapeutics.
Lupus 21st
Century 8Abstract Number: 304 suggesting TRIM21 was acting on this pathway to regulate interferon
production.
Metabolic dysregulation characterizes the tissue response
to immune injury in systemic lupus erythematosus and Conclusion: Taken together our results show that TRIM21 acts as a
inflammatory skin diseases gatekeeper against interferon induction both at a local and systemic
level in response to UV light. This study has important implications
Kathryn Kingsmore for our understanding of how sunlight triggers disease activity
All cells require a source of energy to function. When the demands in some patients and suggest that altered TRIM21 expression or
on a cell change, cells often alter the mechanism by which they activity may explain the link between UV exposure and increased
satisfy their energy demands. In lupus-affected tissues, both the risk of flare in SLE.
immune/inflammatory cells and the resident cells of the tissues
change their energy requirements and monitoring these energy
changes can be an effective means to gauge the overall status of
the tissue. We monitored changes in energy sources in lupus tissues
Abstract Number: 402
by evaluating the expression of genes that control these metabolic
pathways. Herein we observed metabolic changes at the tissue- Genetic Dissection of TLR9 Reveals Complex Regulatory and
level in samples derived from lupus skin or lupus kidney or skin Cryptic Pro-inflammatory Roles
from other inflammatory diseases. To determine whether these Mark J Shlomchik
alterations were a result of changes in immune/inflammatory cell Cardinal lupus autoantibodies to DNA and RNA-associated
metabolism or changes in tissue cell metabolism, we carried out autoantigens (like anti-Sm) depend on so-called “innate immune
extensive bioinformatic analysis. We determined damage to tubule receptors” that bind to DNA and RNA, called TLR9 and TLR7.
cells was most responsible for the observed decreases in metabolism Inhibiting TLR9 and TLR7 is thus an attractive approach for targeted
in lupus kidneys, whereas in skin diseases metabolic changes reflect lupus therapy. However, genetic studies in mouse lupus models
alterations in both immune and non-hematopoietic cells. These showed that blocking TLR9 and TLR7 had opposite effects, with
studies establish a novel way to monitor the metabolic status of blocking TLR9 paradoxically making disease worse, an unexpected
lupus-affected tissues as well as their response to therapy. result. In the studies presented here we made specific mutations in
TLR9 in the genome of lupus-prone mice and analyzed the effects
on disease, which gave insight into how TLR9 both restrains and
400 - INNATE IMMUNITY / promotes lupus-like disease. These studies inform our understanding
of the basic biology of this important innate receptor and it also may
CARDIOVASCULAR DISEASE AND LUPUS provide new leads for therapeutic design.
Abstract Number: 401 Abstract Number: 403
TRIM21 as a Regulator of UVB-Driven IFN Responses in Lupus Bacterial Biofilm Product Curli/eDNA Induces Neutrophil
Caroline Jefferies Extracellular Traps and Serum Anti-Curli/eDNA Levels Correlate
with Bacteriuria and Lupus Activity
Background: Abnormal responses to sunlight or ultraviolet (UV)
light are experienced by approximately two thirds of systemic lupus Roberto Caricchio
erythematosus (SLE) patients, with sun-exposure triggering either Current treatments for SLE patients can diminish active inflammation,
local skin inflammation, or more extensive activation of disease, or but the persistence of the disease and occurrence of flares suggests
both. Recently immune molecules termed type I interferons have that we are underestimating an important pathogenic player. We
been shown to be released locally in response to UV exposure and show here a role for chronic bacteria in the urine in triggering the
drive activation of immune responses both locally and throughout immune system and in doing so, lupus flares. These triggers provide
the body, including the kidneys. However, there is a gap in our the immune system with autoantigens in presence of bacterial
understanding regarding how UV light exposure results in systemic stimuli, chronic bacteria in the urine and common urinary tract
or extensive disease activity in some patients and not others or infections frequent in SLE patients could be the culprit for flares and
healthy individuals. continuous triggering of the lupus autoimmune system.
Results: UV light has multiple effects on cells of the skin, including
inducing DNA damage which can be sensed by DNA-sensing Abstract Number: 404
pathways inside cells, which drive expression of type I interferons.
We previously described a role for the protein TRIM21 as having Platelets Are a Source of Extracellular Mitochondria and
an important role in turning off interferon production. It does so Mitochondrial DNA in Systemic Lupus Erythematosus
by inducing the destruction of key proteins required to induce
responses to DNA and produce interferons. Given the role of TRIM21 Eric Boilard
as a negative regulator of type I interferons, we asked whether lack Extracellular DNA circulating in the blood of patients with lupus
of TRIM21 in mice could result in enhanced sensitivity to UV light. We causes the inflammatory reaction associated with the disease.
found that exposure of wild-type and TRIM21 knockout mice to UV One common denominator of severe forms of the disease is the
light induced similar changes in the skin, however UV-exposed skin presence of anti-DNA antibodies in the blood. It remained unclear
sections from TRIM21 knockout mice had higher levels of antibodies where genetic material was coming from. In this study, we show that
deposited in the skin and higher levels of type I interferon and DNA comes in part from the platelets, better known for their role in
interferon stimulated genes. Most strikingly however, we observed coagulating blood. The DNA is present in the platelet mitochondria,
that TRIM21 knockout animals had enlarged spleens and increased and most of the DNA was actually still inside the mitochondria in the
levels of antibodies and interferon stimulated genes in the blood blood of the patients. This suggests that the body might produce
and organs following UV exposure whereas wild type mice showed antibodies against the mitochondria and the mitochondrial DNA
no such systemic changes. DNA damage is detected in cells by the because it considers them foreign bodies. We propose that the
cGAS-STING pathway. We therefore examined whether this pathway prevention of the release of mitochondria and the mitochondrial
was involved in these enhanced responses to UV exposure in the DNA by platelets might reduce the autoimmune reaction we see
TRIM21 knockout mice. Cells from mice in which both TRIM21 and with this disease.
STING were knocked out showed that in the absence of STING,
loss of TRIM21 failed to result in enhanced UV-driven interferons,
Lupus 21st
9 CenturyAbstract Number: 405 Abstract Number: 503
Does Antimalarial Adherence Decrease the Risk of Cardiovascu- Developing a Standardized Steroid Dosing Regimen in
lar Events and Mortality Among Patients with Incident Systemic Pediatric Proliferative Lupus Nephritis
Lupus Erythematosus and Rheumatoid Arthritis? A Population- Hermine Brunner
Based Study
Corticosteroids (CS) remain the mainstay of therapy for childhood-
Rashed Hoque onset systemic lupus erythematosus (cSLE) although there are
Cardiovascular disease (CVD) is a leading cause of death in patients no widely accepted dosing strategies of oral or intravenous CS.
with inflammatory arthritis, including systemic lupus erythematosus Using an international consensus formation process among 142
(SLE) and rheumatoid arthritis (RA). This population-based study pediatric rheumatologists and nephrologists we developed and
aims to examine the association between antimalarial (AM) initially validated a CS dosing scheme to help standardize the use
adherence and incident CVD events and mortality among newly of CS in children with lupus and lupus nephritis. These pediatric
diagnosed SLE and RA patients. The outcomes were incident CVD rheumatologists and nephrologists achieved > 80% agreement
events and mortality attributed to myocardial infarction, stroke, or that they would use this CS dosing regimen, for their patients.
venous thromboembolism. The exposure was AM adherence with In conclusion, we developed a Standardized Steroid Regimen
three categories based on percentages of prescribed AM doses (SSR) which simulates PO/IV CS use among treating physicians.
are taken: adherence (>90%), partial adherence (0%), The proposed SSR may be useful for clinical care and to regulate
and not taken (=0). We identified 21,114 patients with incident SLE background CS use during clinical trials of new medication for
or RA and incident AM use in British Columbia, Canada, using the children with lupus.
provincial administrative databases between January 1997 and
March 2015. More incident CVD events and CVD mortality were
observed among AM non-adherence and discontinuation than AM Abstract Number: 504
adherence. Using a novel statistical method, this study found that
SLE and RA patients had more than half (53%) and about one third Specific in Situ Inflammatory Architectures Predict Progression
(30%) risk reduction of CVD mortality and incident CVD events when to Renal Failure in Human Lupus Nephritis
adhering to at least 90% of their prescribed AM doses, than when
they took less than 90% of the doses. Marcus Clark
In human lupus nephritis, the nature of the immune response in the
kidney determines if a patient will respond to conventional therapy
or progress to renal failure.
500 - LUPUS NEPHRITIS
Abstract Number: 505
Abstract Number: 501
Parenchymal INFγ Response Regulates Murine Lupus Nephritis
Anti-LG3 Antibodies Contribute to Microvascular Loss and Fi- Jeremy Tilstra
brosis in Lupus Nephritis
Immune cells attacking the kidney are felt to be an important
Mélanie Dieudé contributor to kidney damage (nephritis) in lupus patients. Previously
we showed that the kidney may have self-preservation mechanisms
Systemic lupus erythematosus (SLE) is an autoimmune disease, in in place to prevent optimal activity of these infiltrating immune cells.
which the immune system attacks its own cells and organs. One One hypothesis is that inflammatory mediators secreted by immune
of the organs attacked is the kidney, leading to a kidney disease cells act directly on the kidney cells. The kidneys in response can
called lupus nephritis (LN). During LN, the immune system attacks then alter their function and act to the suppress the infiltrating
the small blood vessels in the kidney leading to improperly filtered immune cells in a feedback loop. The work shown here, supports
waste products from the blood. Kidney transplantation has been this hypothesis in that when immune signaling pathways are
recognized as the most appropriate treatment for those patients, blocked in the kidney tissue alone, but not the immune cells, disease
but several issues remain. Kidney biopsy is the gold standard for as- worsens, suggesting that the kidney has lost its ability to suppress
sessing the condition of the kidney. This invasive procedure carries the infiltrating immune cells. This has significant implications for
great risks. The development of non-invasive methods is needed to therapeutic design and efficacy.
treat LN and kidney attack. Our team has shown that dying vessels
release messengers that can alert the immune system by produc-
ing autoantibodies, antibodies directed against a molecule of the
individual. One of these molecules, LG3, is found on micro-vessels Abstract Number: 506
and autoantibodies directed against LG3, anti-LG3, lead to the loss
of micro-vessels in kidney disease. We show that anti-LG3s contrib- Belimumab Improves Renal Outcomes in Active Lupus Nephritis
ute to the attack on micro-vessels and loss of kidney function in SLE (LN): A Phase 3 Randomized, Placebo-Controlled Trial
mice. A better understanding of the impact of these novel biomark- Brad H Rovin
ers and effector will improve identification, prediction, and manage-
ment of LN. Introduction
Lupus nephritis is an inflammation of the kidneys caused by systemic
lupus erythematosus (SLE), where the body produces antibodies
Abstract Number: 502 that attack its own tissues and organs (autoantibodies). If lupus
nephritis is left untreated, the damage to the cells of the kidneys can
Environmental Adaptation and Tissue Injury in Lupus cause kidney failure and may even result in death.
Joseph Craft Medicines often prescribed for lupus nephritis (standard therapies)
Abrogation of function of T cells and other cells that infiltrate the include high dose corticosteroids and medicines to suppress the
kidneys of patients with lupus (lupus nephritis patients) offers novel immune system, including cyclophosphamide, mycophenolate
therapeutic opportunities. mofetil or azathioprine.
Belimumab is a medicine used to treat SLE; it works by decreasing
the number of autoantibodies that are made by the body. This study
was carried out to understand how well belimumab works when
Lupus 21st
Century 10used to treat lupus nephritis, and how safe belimumab is when with systemic lupus and many will progress to end stage kidney
combined with standard lupus nephritis therapies. disease and death because our current therapies are toxic and often
The study ineffective. This study aims to identify which recently discovered
macrophages that are present in lupus nephritis, but not healthy
The study included 448 patients who were randomly placed into kidneys interact with distinct forms of kidney injury and repair.
one of two groups (224 per group) to receive either belimumab Our findings have the potential to identify which macrophage
or a placebo (a treatment with no medical effect), alongside their subsets mitigate damage or drive repair that can be exploited
standard lupus nephritis treatment. The study was double-blinded, therapeutically. Here, we spatially mapped 3 novel macrophage
so neither doctors nor patients knew who was receiving which types in lupus nephritis kidney sections and discovered that they
treatment. were highly organized in kidney subcompartments and kidney
Results of the study structures. We are now testing whether these novel macrophage
subsets are associated with distinct forms of kidney remodeling.
The researchers were interested in how many patients responded to
treatment. Patients were said to have responded if they continued
taking the treatment for the whole 2 years, and if their kidney
function improved enough, as measured using different medical Abstract Number: 510
tests.
B-cell Interferon-β Correlates with Lupus Nephritis in Systemic
The study found that a greater number of patients in the belimumab Lupus Erythematosus
group responded to treatment compared with patients in the
placebo group. Patients in the belimumab group also had a reduced Walter Winn Chatham
risk of renal events or death compared with those in the placebo Kidney involvement is one of the more serious organ complications
group. of lupus. Autoantibodies associated with kidney disease are derived
Compared with patients in the placebo group, a similar number of from B-lymphocytes, which also play a significant role in the
patients in the belimumab group experienced side effects, however, development of lupus associated autoimmunity. Beta-interferon
fewer patients in the belimumab group experienced serious side is made by B lymphocytes has been shown to be important in
effects. the development of autoimmune B cells and production of B cell
autoantibodies commonly present in patients with lupus nephritis.
What do the results of this study mean? This study shows that high levels of B-cell beta-interferon does not
This study shows that treating patients with belimumab and standard correlate with antibody deposits in the kidney but does correlate
therapy led to better kidney responses compared with placebo and with the development of proliferative nephritis, the more severe
standard therapy, and that there were no unexpected side effects form of lupus kidney disease.
from combining belimumab and standard lupus nephritis therapies.
Abstract Number: 507 Abstract Number: 511
RNAseq Gene Expression Confirms the Importance of GWAS Disease Flares in Lupus Are Concordant with Ruminococcus
Associated Risk Genes in Lupus Nephritis Blautia Gnavus Blooms Arising Within Unstable Gut Microbiota
Communities
Mikhail Olferiev
Gregg J. Silverman
Lupus nephritis (LN) is a severe complication of SLE, but risk genes
predisposing to SLE nephritis are not yet characterized. Here we Systemic Lupus Erythematosus is the archetypic systemic
identified important genes expressed by blood cells that will help autoimmune disease, in which dysbiosis in the gut microbiome
segregate patients with LN and identify the pathogenic mechanisms in genetically-susceptible individuals is postulated to contribute
leading to kidney damage. to pathogenesis. Herein, from longitudinal studies we document
previously unsuspected temporal dynamic instability in these gut-
microbiota communities. We also found there are commonly arising
short-lived blooms of bacterial species with pathogenic properties.
Abstract Number: 508 The most common blooms were of Ruminococcus blautia gnavus,
which occurred in almost half of flares of Lupus nephritis, a severe
C3d-Imaging in Lupus Nephritis form of the disease. Our findings document that there are previously
Joshua Thurman unsuspected shifts within microbiota communities that directly
contribute to serious worsening of autoimmune disease, which we
Currently, the accurate diagnosis of lupus nephritis requires a kidney
postulated is responsible disease flares that often occur in Lupus
biopsy. Biopsies provide invaluable information about how active
nephritis patients despite regular office visits and appropriate
a patient’s disease is, and biopsy results often guide treatment for
treatments. Understanding the microbiome origins of disease
years. Although kidney biopsies are generally safe, however, they
relapse is critical for developing interventions that can attain durable
do require patients to undergo an invasive procedure and they
drug-free remissions.
are susceptible to sample error. We are developing a non-invasive
imaging method to detect inflammation without a biopsy. This
technique (detection of C3d with a radiolabeled probe) provides
a “snapshot” of inflammation throughout the whole body. C3d- Abstract Number: 512
imaging may provide a way to safely monitor patients. This would
allow clinicians to identify patients who need more intensive The Rising Incidence, Prevalence and Mortality Gap of Lupus
treatment. Equally important, it could identify those patients in Nephritis: A Population-Based Study Over Four Decades
whom treatment can reduced or discontinued. Alí Duarte-García
We identified all the patients with lupus nephritis in an 8-county
region from 1976-2018 and estimated how many new cases of lupus
Abstract Number: 509 nephritis occurred over four decades and their outcomes. Over
four decades the number of patients with newly diagnosed lupus
The Localization of Novel Macrophage Subsets in Class III and IV nephritis nearly doubled. Most of the patients are in their thirties at
Lupus Nephritis Kidney Sections the time of diagnosis. There are three times as many women as men
Paul Hoover with lupus nephritis (compare to 8 times as many women as men
with systemic lupus). Patients with lupus nephritis have a six-fold
Lupus nephritis will develop in over 40% of the ~200,000 Americans
Lupus 21st
11 Centuryincrease in the risk of death compared to the general population. Abstract Number: 602
Compared to the general population, the risk of death has increased
in the last four decades. This means that the mortality in the general Longitudinal Cytof Immunophenotyping Reveals Distinct
population has improved more since 1976 than the mortality in Patterns of T Cell-B Cell Dysregulation in SLE
patients with lupus nephritis.
Deepak Rao
This study identified a unique immune cell population expanded in
Abstract Number: 513 early and chronic phases of SLE, which could be a new therapeutic
target of this disease.
Response Gene to Complement -32 Facilitates Local Recruitment
of IL-17- Producing Cells in Immune Complex Mediated
Glomerulonephritis Through the CCR6/CCL20 Axis Abstract Number: 603
Violeta Rus
Autoreactivity Drives Increased Metabolism in T cells from SLE
Response Gene to Complement (RGC)-32 is a molecule localized Patients?
inside many cell types. It controls their multiplication, activation and
migration into tissues. In mice with lupus nephritis, it promotes the Jeroen Roose
infiltration of cells that can cause kidney damage. Blocking RGC-32 In autoimmune diseases, like Lupus, immune cells are wrongfully
in these mice prevents the damage induced by damaging cells. Thus, instructed to attack our own body (termed “self”). Exactly how
RGC-32 is a potential therapeutic target in lupus nephritis. recognition of self by immune cells causes immune cells to spin
out of control is not known. In the Roose lab we have uncovered
a novel “instructive signal” that one type of immune cells, called T
Abstract Number: 514 cells, receive when these T cells see self. We have identified players
in this “instructive signal” using novel (single cell) technologies and
Voclosporin For Lupus Nephritis: Interim Analysis of the mouse models and we have determined that these T cells enter an
AURORA 2 Extension Study unwanted, elevated energetic state with increased cell metabolism.
When we inhibit one of these targets in this novel instructive signal
Simrat Randhawa in a mouse model of autoimmune disease, we cure the mouse. We
In clinical trials, voclosporin in combination with mycophenolate are now capitalizing on our insights and novel technologies and
mofetil (MMF) and low-dose steroids reduced the amount of protein are transitioning to studying patients. We aim to set up a research
in the urine at one year of treatment in adults with lupus nephritis. program in which we collaborate with clinicians and industry to
The AURORA 2 study is evaluating long-term use of voclosporin eventually enable targeting of this novel, instructive metabolic
compared to placebo, in combination with MMF and low-dose signal in T cells of autoimmune patients.
steroids, for an additional two years of treatment. An interim analysis
of the AURORA 2 study will be presented.
700 - MACROPHAGE IN SLE
600 - T CELLS
Abstract Number: 701
Abstract Number: 601 Therapy of Diffuse Alveolar Hemorrhage in Experimental Lupus
With Recombinant Myxomavirus Protein Serp-1
An Imbalance Between Regulatory and Pro-Inflammatory T Westley Reeves
Cell Subsets Distinguishes Symptomatic from Asymptomatic
Individuals with Anti-Nuclear Antibodies Lung hemorrhage is fatal in over half of SLE patients with this
complication. At present, there are no clearly effective treatments.
Joan Wither We developed a mouse model of lupus with lung hemorrhage and
Antinuclear antibodies (ANAs) are a characteristic feature of lupus, found that macrophages play a central role. Rabbit myxomavirus
but are also found in healthy people, only a small subset of whom produces an immunomodulatory protein (Serp-1) that enhances
will eventually develop disease. Currently the immune features viral infectivity by impairing the host’s macrophage function.
the distinguish people who have ANAs without symptoms from Recombinant Serp-1 prevented lung hemorrhage in lupus mice
those with lupus and other similar autoimmune diseases, or that and normalized the low expression levels of macrophage reverse
can be used to predict the subset of people with ANAs who will cholesterol transporter ABCA1 seen in SLE. Individuals with ABCA1
develop disease, are largely unknown. In this study we compared mutations develop early onset severe atherosclerosis, suggesting
the blood immune cell populations in asymptomatic people that the lupus-related ABCA1 deficit may contribute to accelerated
with ANAs with those who had early symptomatic disease. We atherosclerosis. Thus, Serp-1 may warrant further study for treating
found that asymptomatic people with ANAs have many immune both lung hemorrhage and accelerated atherosclerosis in SLE.
changes indicating abnormal activation of their immune system
as compared to healthy people lacking these antibodies. However,
the immune cell populations that regulate the immune system and Abstract Number: 702
help to prevent autoimmune disease are also expanded in these
individuals. This expansion is not found in people with early disease, Pristane Induced Lupus in HDAC6-Mice
where increases in the cells that support production of inflammation
causing antibodies are seen. Our findings suggest that in people Christopher M. Reilly
with ANAs that lack symptoms the immune system actively inhibits Histone deacetylase 6 (HDAC6) is an enzyme that acetylates many
development of disease and that in patients with disease this proteins altering their activation. We sought to determine if HDAC6
inhibition is defective, allowing inflammation to develop. inhibition would prevent activation of inflammation in the pristine
induced lupus mouse model. We found that HDAC6 inhibition alters
the expression of several interferon genes that are activated in lupus.
Lupus 21st
Century 12800 - PHARMACOEPIDEMIOLOGY 1000 - PATIENT-REPORTED OUTCOMES
Abstract Number: 801 Abstract Number: 1001
Factors Associated with SLE Flares After HCQ Taper, Longitudinal Changes in Type 2 SLE Activity
Discontinuation or Maintenance in the SLICC Inception Cohort: Amanda Eudy
Lower Education Linked with Higher Flare Risk
Patients with lupus experience Type 2 SLE symptoms such as fatigue
Sasha Bernatsky differently over time, with some having persistently high or low
Hydroxychloroquine (HCQ) is a key drug in lupus, which can reduce Type 2 activity and others having variable severity. Future studies
the risk of serious disease flares. However, there are increasing will determine if this fluctuation is due to inflammation or non-
concerns about irreversible eye damage, the main side effect with inflammatory etiologies such as perceived stress, extent of social
long-term use of this drug. HCQ can be reduced or discontinued support, PTSD, illness perception, or resilience factors.
in order to avoid side effects. Although some patients do well
after reducing or discontinuing the drug, others may have serious
flares. Thus, we evaluated how the risk of flare differ by individual Abstract Number: 1002
characteristics among patients reducing or stopping HCQ, compared
to those remaining on the drug. We observed that patients using The Mitigating Effects of Self-Efficacy on Pain Interference
prednisone or immunosuppressor agents have more chances of Differ by Depression in Black Women with Systemic Lupus
flaring in either circumstance of HCQ use. On the other hand, patients Erythematosus
without a post-secondary education could be at a particular risk of
flaring if HCQ is discontinued. These disparities should be addressed Cristina Drenkard
in order to enable all lupus patients to benefit from personalized Systemic lupus erythematosus (SLE) is an autoimmune chronic
decision-making and improved outcomes. disease that disproportionately strikes young women and Black
individuals. SLE can potentially affect every organ system with a
variety of symptoms.
900 - NUCLEIC ACIDS IN SLE Pain is a pervasive and distressing symptom reported by people
living with SLE, even by those who have the disease under control.
Self-efficacy can help mitigate the negative effect of pain on daily
Abstract Number: 901 activities; however, some studies suggest an inverse relationship
between self-efficacy and depression. We examined whether self-
efficacy affects pain interference in Black women with SLE and
Autoantibody-Mediated Impairment of DNASE1L3 Activity in whether depression alters those relationships.
Sporadic Systemic Lupus Erythematosus
We found an inverse association between pain interference and
Boris Reizis self-efficacy (to manage symptoms and to manage medications
Systemic lupus erythematosus (SLE) is associated with aberrant and treatments). However, depression, a highly prevalent and
immune response to the body’s fundamental building block, the often underdiagnosed condition in patients with SLE, reduced the
DNA. We found that in patients with severe SLE, the activity of beneficial effect of self-efficacy to control pain interference in Black
a key enzyme that destroys self-DNA is reduced, leading to the women with this condition.
accumulation of self-DNA in circulation. Paradoxically, this enzyme Clinicians serving SLE patients should be aware of the negative
itself was blocked by antibodies, showing that the immune system impact of depression on self-efficacy, which in turn can affect pain
attacks the key guardian of tolerance to DNA and this perpetuates interference control. Programs designed to build self-efficacy should
autoreactivity. This vicious cycle represents an important target for consider these findings to maximize intervention effectiveness.
emerging therapeutic approaches to the disease.
Abstract Number: 1003
Abstract Number: 902
Race, Ethnicity and Patient-Reported Outcomes in Childhood
Regulatory RNAs in Neuropsychiatric Systemic Lupus Onset Systemic Lupus Erythematosus
Erythematosus
Ezequiel Borgia
Henri Tiedge
This study examined whether self-reported outcomes vary across
Neuropsychiatric lupus is an enigmatic disease in which the racial/ethnic groups in children with lupus using data from a
nervous system is impacted by autoantibodies. We have identified national registry of pediatric rheumatic diseases.
lupus autoantibodies that are directed against brain regulatory
RNAs which control the function of synaptic connections between
nerve cells. These autoantibodies prevent the RNAs from being
transported to such synapses and thus from functioning there. As a 1100 - CLINICAL RESEARCH IN SLE
result, neuronal networks become excessively excitable. We propose
that this mechanism is causal to neuropsychiatric manifestations in
lupus patients, manifestations that include seizures and cognitive
impairment. Our data also suggest that we can prevent lupus
Abstract Number: 1101
autoantibodies from eliciting such manifestations and that we may
therefore be able to offer treatment options to patients. Use of Popular Opinion Leader Models to Disseminate
Information About Clinical Trials to People of Color with Lupus
in Two U.S. Cities
Rosalind Ramsey-Goldman, Candace H. Feldman
Despite the increased burden of lupus and adverse outcomes among
Black compared to White individuals with lupus, people of color are
underrepresented in lupus clinical trials. We leveraged a community-
Lupus 21st
13 Centuryacademic partnership in two U.S. cities to design and implement a Abstract Number: 1104
program where we trained trusted individuals with large social
networks (“Popular Opinion Leaders”, POLs) about clinical trials Update on the Study of Anti-Malarials in Incomplete Lupus
and they disseminated this information through their communities Erythematosus (SMILE) clinical trial
and networks. We measured increase in POL knowledge and their
reach. We found that POLs’ knowledge improved after receiving the David Karp1*, Nancy Olsen2, Duanping Liao2, Judith James3, Cristina
training and successfully disseminated information virtually, given Arriens3, Diane Kamen4, Mariko Ishimori5, Susan Boackle6.
pandemic restrictions, with substantial reach. Further studies are Systemic lupus erythematosus develops in a fraction of the people
needed to determine whether this approach increases diversity in who are at risk based on genetic, hormonal, and environmental
clinical trial enrollment. factors. Why some develop lupus, and others do not, is unknown.
It has been shown previously that there are changes in the immune
system at least five years before a lupus diagnosis is made, and
Abstract Number: 1102 clinical features (rash, arthritis) typically occur 1-2 years before
diagnosis. This clinical trial has enrolled people at risk for lupus who
Fish Oil Supplementation and Pro-Inflammatory and Pro- have evidence of autoimmunity and some early signs or symptoms
Resolving Lipid Mediators in Patients with and Without of disease but are not yet sick enough to need treatment. We are
Systemic Lupus Erythematosus testing whether the drug, hydroxychloroquine, which is known to
treat lupus, can prevent these people from developing more signs
Karen H. Costenbader and symptoms. In this study, we hope to learn whether lupus can be
When fish oil supplements are ingested, they are broken down prevented, and by analyzing their immune systems, discover better
into smaller particles by the body. Some of these particles ways to predict who will get lupus in the future.
promote inflammation (pro-inflammatory) while others are called
“specialized pro-resolving mediators” (SPM) because they reduce
inflammation. Since inflammation is high in lupus patients, we Abstract Number: 1105
wanted to understand the level of these particles in lupus patients
who take fish oil supplements. In this study, we compared 16 Telemedicine in Rheumatology: A Survey of Patient and Provider
lupus patients on fish oil to 16 lupus patients not on fish oil. As a Satisfaction with Virtual Care
comparison group, we also recruited 16 nonlupus patients on fish
oil and 16 non-lupus patients without fish oil so that they were Anca Askanase
similar in age, sex, and race to the lupus patients. We showed that Telemedicine has accelerated its popularity among patients and
lupus patients on fish oil had lower levels of pro-inflammatory providers during the COVID-19 pandemic but there has been a
particles compared to lupus patients not taking fish oil, while the relative paucity of research evaluating its role in rheumatology
opposite was seen in the non-lupus comparison. However, when practice. Our single-center rheumatology patient cohort with a high
we considered how sick the lupus patients were, there was no burden of complex Systemic Lupus Erythematosus (SLE) showed a
difference in pro-inflammatory or SPM levels. This maybe because high rate of satisfaction with virtual care in the video-conference
lupus patients inherently have higher levels of inflammation, or they format compared with conventional in-person visits.
cannot make SPMs. As this was a small study based on information
obtained from health records, larger studies controlling the type of
fish oil, doses, and compliance are still needed. Abstract Number: 1106
Predicting Adverse Pregnancy Outcomes in Women with
Abstract Number: 1103 Systemic Lupus Erythematosus: A Comparison of Machine
Learning Methods
Perfluoroalkyl Substances and Community Vulnerability:
Mimi Kim
Associations with Lupus-Related Autoantibodies and Disease
Nearly 20% of pregnancies in patients with Systemic lupus
Diane Kamen
erythematosus (SLE) result in an adverse pregnancy outcome (APO);
There are numerous potential environmental exposures that can early identification of women with SLE who are at high risk of APO
influence the progression from autoimmunity to systemic lupus is vital. We previously developed a prediction model for APO using
erythematosus. Perfluoroalkyl substances (PFAS) are potential data from the PROMISSE Study, a large multi-center, multi-ethnic/
environmental triggers under investigation. PFAS are found in many racial study of APO in women with mild/moderate SLE and/or aPL.
products, including nonstick products, water repellant fabrics, fire- While our initial model showed promising predictive performance,
retardant foams, and food packaging. They are associated with we sought to determine if novel and increasingly popular machine
negative health effects by causing hormone disruption and immune learning approaches would enhance APO risk prediction using all
dysfunction. This ongoing study explores the associations between available predictors and potential complex relationships between
PFAS exposure, measures of autoimmunity, and neighborhood/ them. We found that several popular ML algorithms did not provide
individual-level social determinants of health among African meaningful improvements in the prediction of APO over simpler
Americans participating in a population-based cohort study. Our regression-based methods. New clinical and laboratory markers may
study included 81 African American participants (10 patients with be needed to improve predictions in the future.
lupus and 71 participants without lupus). We evaluated blood levels
of two types of PFAS (perfluorooctanesulfonic acid (PFOS) and
perfluorooctanoic acid (PFOA)) and found a significant association Abstract Number: 1107
between PFOS exposure and neighborhood/individual vulnerability.
We also found a significant association between presence of a
Economic Evaluation of Hydroxychloroquine Use in an
positive antinuclear antibody (ANA) test, as a screening test for
International Inception Cohort
autoimmunity, and neighborhood/individual vulnerability.
Ann Clarke
Patients with lupus have high financial costs related to their
disease. Hydroxychloroquine is the foundation medication for
lupus treatment. While its ability to help treat lupus and prevent its
complications is well-understood, not much is known about whether
patients who use hydroxychloroquine have lower health care costs
than those who do not. This study of almost 700 international lupus
Lupus 21st
Century 14You can also read
