Judith & Stewart Colton Center for Autoimmunity

At NYU Langone’s Judith and Stewart Colton Center for Autoimmunity, physicians and scientists collaborate on research to better understand the immunological basis of autoimmunity and develop new diagnostic tools and treatments for people with autoimmune diseases.
Autoimmune diseases arise when the human immune system mistakenly recognizes and attacks normal parts of the human body as if they were "foreign". Such autoimmune response may be directed towards specific cell types, resulting in organ-specific diseases such as type I diabetes or multiple sclerosis. It may also be directed against common cellular components such as DNA and RNA, resulting in systemic autoimmune diseases such as systemic lupus erythematosus. The incidence of all autoimmune diseases has been steadily rising in the last decades, emphasizing the urgent need for better understanding and treatment of these diseases.
We integrate science and technology, and encourage a collaborative culture between basic science researchers, data scientists, and clinicians of diverse expertise. Our aim is to foster transformative discoveries about the environmental triggers and immunological events that characterize autoimmune disease onset.
Our approach to translational research builds on a tradition of strong basic and clinical sciences, and well-characterized patient cohorts. Studies from the Judith and Stewart Colton Center for Autoimmunity have investigated a number of autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Behcet’s syndrome, inflammatory bowel disease, multiple sclerosis, and myasthenia gravis.
Contact Us
For inquiries, please contact Jennifer Gillen at JenniferA.Gillen@NYULangone.org. For patient care questions, please check out the areas of expertise for immune system disorders.
Research

Advances in Autoimmunity Symposium

Dr. Carla Nowosad Receives Michelson Prize
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Structural Insights Reveal Interplay Between LAG-3 Homodimerization, Ligand Binding, and Function
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Transmembrane Domain–Driven PD-1 Dimers Mediate T Cell Inhibition
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IFN-γ–producing TH1 cells and dysfunctional regulatory T cells contribute to the pathogenesis of Sjögren’s disease
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