1. TIGIT stimulation suppresses autoimmune uveitis by inhibiting Th17 cell infiltration.
- Author
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Peters K, McDonald T, Muhammad F, Brady A, Dostal J, and Lee DJ
- Subjects
- Animals, Mice, Mice, Inbred C57BL, Disease Models, Animal, Uveitis immunology, Uveitis pathology, Th17 Cells immunology, Receptors, Immunologic metabolism, T-Lymphocytes, Regulatory immunology, Autoimmune Diseases immunology, Autoimmune Diseases pathology
- Abstract
T cell immunoglobulin and ITIM domain (TIGIT) is an immune checkpoint molecule that suppresses T cell activation and promotes an immunosuppressive environment to suppress autoimmune diseases. However, the impact of a TIGIT agonist as a treatment for ocular autoimmune disease has not been investigated. We examined TIGIT expression on T helper 17 (Th17) and regulatory T cells (Tregs), the role of TIGIT on experimental autoimmune uveitis and Th17 cells, and the impact of Treg generation following TIGIT stimulation. TIGIT stimulation at the onset of clinical symptoms reduced the severity of uveitis and suppressed infiltration of Th17 cells into the eye. Further, Tregs from mice treated with the TIGIT agonist were capable of suppressing experimental autoimmune uveitis in recipient mice. This report demonstrates that stimulation of TIGIT at onset of disease suppresses symptoms and allows for induction of regulatory immunity that provides resistance to uveitis., Competing Interests: Conflict of interest statement. None declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Leukocyte Biology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)
- Published
- 2024
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