Lupus Research Alliance Awards Lupus Insight Prize for Critical Discovery of TLR7 Immune Control Sensor Failure Driving Lupus

Prize Bestowed to Gregory Barton, PhD, University of California, Berkeley, and Howard Hughes Medical Institute, and Olivia Majer, PhD, Cincinnati Children's

NEW YORK, Nov. 11, 2026 /PRNewswire/ -- The Lupus Research Alliance, the world's largest private funder of lupus research, proudly awarded the 2026 Lupus Insight Prize to Gregory Barton, PhD, University of California, Berkeley, and Howard Hughes Medical Institute, and Olivia Majer, PhD, Cincinnati Children's, during ACR Convergence 2026 (November 6-11, Orlando), the annual meeting of the American College of Rheumatology. The Prize recognizes Drs. Barton and Majer's defining work revealing how UNC93B1, a key regulator of the immune system's RNA‑sensing receptor TLR7, normally keeps immune responses in check and how genetic changes in this pathway can lead to disease, pointing to new opportunities for targeted treatments.

The Lupus Insight Prize is a signature honor of the Lupus Research Alliance, now in its 14^th year, that awards $100,000 for a recent, seminal lupus discovery that shifts understanding or treatment of the disease. Co-recipients Dr. Barton and Dr. Majer were awarded the Prize during the ACR Convergence 2026 during the newly established Lupus Research Alliance Lupus Insight Prize Lectureship.

During a session moderated by Gary Koretzky, MD, PhD, Cornell University, Drs. Barton and Majer presented their seminal findings to an esteemed audience of clinicians, researchers, and members of the scientific community.

"The Lupus Insight Prize recognizes discoveries that have the power to transform how we understand and treat this complex disease," said Teodora Staeva, PhD, Chief Scientific Officer at the Lupus Research Alliance. "The work of Drs. Barton and Majer provides compelling insight into how the immune system loses its ability to distinguish self from non-self in lupus and helps identify patients who may benefit from therapies targeting the TLR7 pathway."

Uncovering the Missing Link Between TLR7 Dysregulation and Lupus

TLR7 is an immune sensor that helps the body detect viral infections by recognizing genetic material (RNA) from viruses. Because similar genetic material is present in the body's own cells, TLR7 must be tightly controlled to prevent it from mistakenly targeting healthy tissue. This control is partly managed by UNC93B1, a protein that directs where TLR7 travels inside cells and helps regulate when and where it can signal. Although abnormal TLR7 activity is recognized as a major driver of lupus, exactly how UNC93B1 restrains this pathway — and how its disruption leads to disease — had previously remained unclear.

In a landmark 2024 study, Dr. Barton and his team, which included Dr. Majer during her postdoctoral training, performed the first systematic analysis of UNC93B1 — testing the effects of more than 100 genetic mutations across the protein. The team identified dozens of variants that increase TLR7 activity — far more than expected — and showed that several of these same mutations are present in individuals with lupus. Importantly, mice engineered to carry these mutations developed severe lupus-like disease, showing that disruption of UNC93B1 can directly drive autoimmunity.

"We were surprised by how many mutations in UNC93B1 could amplify TLR7 activity," said Dr. Barton, whose work has been previously funded by several Lupus Research Alliance grants. "Our findings reveal just how precisely this pathway must be controlled— and how even small changes can push the immune system toward disease."

Building on these findings in her own lab, Dr. Majer uncovered how a disease-causing UNC93B1 mutation works at a molecular level in a child with early-onset lupus. Her findings revealed that UNC93B1 normally partners with a cellular complex called BORC to help ensure that activated TLR7 is properly degraded once its job is done. The lupus-associated mutation disrupts this process, allowing TLR7 to accumulate inside immune cells and become overly responsive to the body's own RNA.

Together, these studies establish UNC93B1 as a critical safeguard that keeps TLR7 activity in check. Dr. Barton's work maps the landscape of UNC93B1 mutations that can drive excessive immune activation, while Dr. Majer's studies explain how defects in this pathway lead to disease at the molecular level. Collectively, their findings deepen understanding of how immune balance is maintained and provide a foundation for more precise approaches to diagnosing and treating lupus by restoring proper TLR7 regulation.

"Understanding this pathway and its role in lupus development will help provide patients with a more definitive diagnosis and identify better opportunities for therapeutic intervention," Dr. Majer said. "If we can identify patients with these specific mutations, we can begin to match them with therapies that more directly target the underlying cause."

Dr. Barton is Co-Chair of the Department of Molecular and Cell Biology at the University of California, Berkeley, a Howard Hughes Medical Institute Investigator, and C.H. Li Distinguished Professor of Immunology and Molecular Medicine. Dr. Majer is an Associate Professor of Immunology in the University of Cincinnati Department of Pediatrics and leads an Immunobiology lab at Cincinnati Children's. She previously conducted postdoctoral research in Dr. Barton's laboratory at UC Berkeley.

To learn more about the Lupus Insight Prize and past honorees, visit here.

About Lupus
Lupus is a chronic, complex autoimmune disease that affects millions of people worldwide. In lupus, the immune system, meant to defend against infections, produces autoantibodies that mistake the body's own cells as foreign, causing other immune cells to attack organs such as the kidneys, brain, heart, lungs, and skin, as well as blood and joints. Ninety percent of people with lupus are women, most often diagnosed between the ages of 15-45. Black, Latinx, Indigenous, Asian and Pacific Islander people are disproportionately affected by lupus.

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 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 go to support lupus research programs.

For more information or to donate to lupus research, visit the LRA at LupusResearch.org and on social media at: X, Facebook, LinkedIn, and Instagram.

SOURCE Lupus Research Alliance