Judith Ashouri Sinha, MD
Associate Professor
Medicine
School of Medicine

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.

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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.

Awards

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  • NIH R01 Award, NIAMS, 2025-2030
  • Nora Eccles Treadwell Foundation Award in Arthritis Research, Nora Eccles Treadwell Foundation, 2025-2029
  • Nora Eccles Treadwell Foundation Award in Arthritis Research, Nora Eccles Treadwell Foundation, 2022-2025
  • NIH K08 Award, NIAMS, 2018-2023
  • 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

Education & Training

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  • Fellowship Rheumatology University of California, San Francisco 06/2014
  • Residency Internal Medicine Stanford University Hospital & Clinics 06/2011
  • MD University of California, San Francisco 06/2008

Interests

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  • Pathogenic T cell signaling in rheumatoid arthritis
  • Rheumatology
  • Autoimmunity
  • Immunology

Websites

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Grants and Projects

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Publications (20)

Top publication keywords:
Th17 CellsNuclear Receptor Subfamily 4, Group A, Member 1Autoimmune DiseasesArthritis, ExperimentalArthritis, RheumatoidSynovial MembraneZAP-70 Protein-Tyrosine KinaseParaneoplastic SyndromesAntiphospholipid SyndromeProtein-Tyrosine KinasesCD4-Positive T-LymphocytesAutoimmunityReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-CellVasculitis

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