Judith Ashouri Sinha, MD

Assistant Professor

Rheumatoid arthritis (RA) afflicts millions globally, causing significant joint deformity, pain, and functional disability. RA is without cure and its cause is unknown, but CD4 T cells—immune cells widely accepted to play a key role in RA pathogenesis—from patients with RA become activated by proteins through their T cell receptor (called “antigen-specific T cells”) and cause arthritis. Dr. Ashouri’s research uses a unique tool to identify and characterize these antigen-activated T cells in both a mouse model of RA and human RA. Elucidating the contribution of these pathogenic CD4 T cells to arthritis development in RA holds promise for the discovery of improved therapeutic targets.
Fellowship, 06/2014 - Rheumatology, University of California, San Francisco
Residency, 06/2011 - Internal Medicine, Stanford University Hospital & Clinics
MD, 06/2008 - , University of California, San Francisco
Honors and Awards
  • Arthritis National Research Foundation Scholar, Arthritis National Research Foundation, 2018-2020
  • K Bridge Award, Rheumatology Research Foundation, 2017-2018
  • Bechtel Junior Faculty Award, UCSF Division of Rheumatology, 2016-2019
  • Scientist Development Award, Rheumatology Research Foundation, 2012-2015
  1. Reporters of TCR signaling identify arthritogenic T cells in murine and human autoimmune arthritis.
  2. Endogenous Nur77 Is a Specific Indicator of Antigen Receptor Signaling in Human T and B Cells.
  3. A sharp T-cell antigen receptor signaling threshold for T-cell proliferation.
  4. A young woman with systemic lupus erythematosus and extensive mesenteric vasculitis involving small and medium vessels.
  5. Rheumatic manifestations of cancer.
  6. Transcriptional regulation of EGR-1 by the interleukin-1-JNK-MKK7-c-Jun pathway.
  7. Androgens are protective in experimental autoimmune encephalomyelitis: implications for multiple sclerosis.
  8. Estrogen receptor alpha mediates estrogen's immune protection in autoimmune disease.