Related Experiment Video
Updated: Jun 25, 2025

Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
TIGIT stimulation suppresses autoimmune uveitis by inhibiting Th17 cell infiltration
Kayleigh Peters1, Trisha McDonald1, Fauziyya Muhammad2
1Department of Ophthalmology/Dean McGee Eye Institute, University of Oklahoma Health Sciences Center, 608 Stanton L Young Blvd, Oklahoma City, OK 73104, United States.
None:
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.
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Tumor Immunotherapy

