NEW YORK, NY, May 23, 2024 — The Lupus Research Alliance (LRA) is proud to announce that nine international researchers are the recipients of this year’s Lupus Innovation Award (LIA). They will conduct innovative research to uncover the underlying mechanisms and identify novel targets and pathways that could be harnessed to predict, monitor, and treat lupus, a complex autoimmune disease. The LIA provides investigators up to $150,000 per year for two years and aims to enable the development of more effective and safer therapies and address major barriers in lupus research.

Systemic lupus erythematosus (SLE) can affect several parts of the body and varies widely from person to person, often with severe complications. Current therapy involves mostly non-specific anti-inflammatory and immunosuppressive drugs. While these treatments are often beneficial, many patients may not see much improvement or suffer harmful side effects. The LIA supports pioneering approaches to these significant challenges in lupus research.

“We are pleased to award nine recipients of the 2023 Lupus Innovation Award”, noted Teodora Staeva, Ph.D., Vice President and Chief Scientific Officer of the LRA. “The latest group of LRA grant recipients will address a number of outstanding questions with the potential to lead to new treatments and tools to better diagnose and monitor disease progression for people with lupus.”

Recipients of the 2023 Lupus Innovation Award:

New Types of Cell Therapies to Target Disease-Causing B Cells

Laura Belver, Ph.D., Josep Carreras Leukaemia Research Institute, Spain

People with lupus often have anti-DNA autoantibodies –produced by B cells– that mistakenly recognize their own DNA as a foreign invader. These autoantibodies can build up in the kidneys and other organs, causing inflammation, damage, and reduced function. Dr. Belver will develop a chimeric autoantibody receptor (CAAR)-based cell therapy to eliminate B cells that produce anti-DNA autoantibodies. This method will remove disease-causing B cells while sparing healthy B cells, providing a safe and effective treatment for people with SLE.

Maria Tokuyama, Ph.D., University of British Columbia, Canada

Endogenous retroviruses (ERVs) are like fossils of ancient viral infections that have become part of our DNA. In people with lupus, B cells can produce autoantibodies that mistakenly target ERV proteins, leading to inflammation and kidney damage. Dr. Tokuyama and her colleague Dr. Laura Evgin will develop a new type of CAAR T-cell that specifically eliminates ERV-targeting B cells, leaving healthy B cells intact. She will then test whether this novel strategy can reduce disease development and progression in a mouse model of lupus.

Uncovering Underlying Factors of Devastating Pregnancy Complications in SLE

Lisa van Baarsen, Ph.D., University of Amsterdam, the Netherlands

Lupus typically affects women during childbearing years. Pregnancies in women with SLE are often associated with a higher risk of maternal complications, like preeclampsia (a severe blood pressure condition). There is also a high risk of devastating fetal outcomes like preterm delivery, growth restriction, and even fetal loss. Dr. van Baarsen and colleague Dr. Wendy Dankers will explore how a process necessary for a healthy pregnancy, called maternal-fetal tolerance — meaning the pregnant woman’s immune system accepts the growing baby as a part of her own body rather than a foreign body– is disrupted in SLE. Findings from this study could improve the way we predict, treat, and prevent pregnancy complications in women with lupus.

Anne Davidson, M.B.B.S., The Feinstein Institutes for Medical Research, United States

Antiphospholipid antibodies are responsible for approximately 4 percent of stillbirths in the general population and contribute to the increased risk for poor pregnancy outcomes in people with SLE. Dr. Davidson developed a mouse model of pregnancy loss induced by antiphospholipid antibodies to test whether TLR8, a molecule that acts as a sensor for the immune system, is responsible for developmental problems in the placenta and if TLR8 can be targeted to improve pregnancy outcomes for women with SLE.

 Finding the “Tipping Point” that Drives B Cells from Helpful to Harmful in SLE

Federico Gaiti, Ph.D., University Health Network, Canada

In SLE, B cells can become self-reactive, producing autoantibodies that mistakenly target a person’s own cells as foreign invaders. The factors that drive disease development and the ability of self-reactive B cells to promote lupus are not well understood. With colleagues Drs. Leandro Venturutti and Zahi Touma, Dr. Gaiti will characterize the changes in B cells that promote SLE at extremely high resolution and investigate the genetic and immune factors that worsen the disease. These findings could highlight biomarkers for early detection and potential targets for eliminating disease-causing B cells.

Developing a Novel Tool to Improve Lupus Nephritis Diagnosis

Aaron Morris, Ph.D., The Regents of the University of Michigan, United States

Kidney inflammation caused by lupus, called lupus nephritis (LN), is a dangerous complication of SLE that is hard to predict, detect, monitor, and treat. Common tests like blood and urine testing are not sensitive enough to detect all cases of LN, while surgical kidney biopsies are invasive and cannot be repeated often, highlighting the need for new technologies to diagnose LN. Dr. Morris will develop a novel diagnostic tool that is less invasive than surgical kidney biopsies which could accelerate LN diagnosis and make it easier to select the right treatment, predict a flare, and monitor response to treatment.

Understanding the Underlying Causes of SLE

John Ray, Ph.D., Benaroya Research Institute at Virginia Mason Franciscan Health, United States

Although we do not understand what exactly causes SLE, research has identified over 150 areas of the genome, or genetic map, associated with lupus. However, most genetic differences between people, called variants, that correlate with SLE occur in genome regions we know little about.  Dr. Ray will identify genetic variants that alter B cell activation, function, and gene regulation (how a cell controls which genes are expressed) to prioritize the variants that likely cause SLE and identify targets for future therapies.

Tarin Bigley, M.D., Ph.D., Washington University, United States

While the causes of SLE are unclear, studies suggest that environmental exposures, like viral infections, play a key role. Roseolovirus, a kind of herpes virus that has infected more than 90 percent of adults in the general population, has been associated with SLE, but understanding how roseolovirus infection leads to SLE has been challenging due to the long period between the initial infection and when lupus symptoms first develop. Dr. Bigley will study how early-life roseolovirus infection results in immune cell alterations and autoimmunity in SLE.

Using Immune Cell Changes to Predict Response to Therapy

 Marta E. Alarcón-Riquelme, M.D., Ph.D., Fundacióon Publica Andaluza Progreso y Salud, Spain

While new treatments for SLE have been developed and show promise in clinical trials, not all people with SLE respond to treatment. This may be due to the heterogeneity of lupus — how it differs from person to person. Dr. Alarcon-Riquelme will group people with SLE based on how they respond to treatment and explore which immune cells change when a person responds or does not respond to therapy and what genes these cells have that make them unresponsive to therapy. The team will then see if they can use these findings to predict a person’s response to treatment.

About Lupus
Lupus is a chronic, complex autoimmune disease that affects millions of people worldwide. More than 90 percent of people with lupus are women, often striking during the childbearing years of 15-45. Black, Hispanic, Indigenous, and Asian/Pacific Islander people are disproportionately affected by lupus and are more likely to experience severe lupus symptoms. In lupus, the immune system, meant to defend against infections, produces antibodies that mistakenly recognize the body’s own cells as foreign, prompting other immune cells to attack and potentially damage organs such as the kidneys, brain, heart, lungs, blood, skin, and joints.

About the Lupus Research Alliance
The Lupus Research Alliance is the largest non-governmental, non-profit funder of lupus research worldwide. The organization aims to transform treatment by funding the most innovative lupus research, fostering diverse scientific talent, and driving discovery toward better diagnostics, improved treatments and ultimately a cure for lupus. Because the Lupus Research Alliance’s Board of Directors funds all administrative and fundraising costs, 100% of all donations goes to support lupus research programs.  For more information, please visit the LRA at LupusResearch.org and on social media at:  X, Facebook, LinkedIn, and Instagram.