Judith Ashouri Sinha, MD
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
- Reporters of TCR signaling identify arthritogenic T cells in murine and human autoimmune arthritis.
- Endogenous Nur77 Is a Specific Indicator of Antigen Receptor Signaling in Human T and B Cells.
- A sharp T-cell antigen receptor signaling threshold for T-cell proliferation.
- A young woman with systemic lupus erythematosus and extensive mesenteric vasculitis involving small and medium vessels.
- Rheumatic manifestations of cancer.
- Transcriptional regulation of EGR-1 by the interleukin-1-JNK-MKK7-c-Jun pathway.
- Androgens are protective in experimental autoimmune encephalomyelitis: implications for multiple sclerosis.
- Estrogen receptor alpha mediates estrogen's immune protection in autoimmune disease.