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Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • T cell Ig and ITIM domain (TIGIT) is a receptor on T cells that binds CD155 on dendritic cells.
  • TIGIT has an ITIM motif and is implicated in autoimmune disease via the TIGIT/CD226 pathway.

Purpose of the Study:

  • To investigate the specific role of TIGIT in human CD4(+) T cells.
  • To elucidate the mechanism of TIGIT-mediated T cell regulation.

Main Methods:

  • Utilized an agonistic anti-TIGIT monoclonal antibody (mAb) to assess T cell proliferation and cytokine production.
  • Employed short hairpin RNA (shRNA) to knock down TIGIT expression and analyzed gene and protein expression.
  • Investigated the impact of blocking CD226 signaling on TIGIT-mediated effects.

Main Results:

  • Direct inhibition of T cell proliferation and decreased expression of T-bet, GATA3, IRF4, and RORc observed with anti-TIGIT mAb.
  • Inhibition of predominantly IFN-γ production.
  • TIGIT knockdown increased T-bet and IFN-γ expression while decreasing IL-10.
  • Increased IFN-γ upon TIGIT knockdown was reversed by blocking CD226 signaling.

Conclusions:

  • TIGIT inhibits T cell functions both by competing with CD226 for CD155 and through T cell-intrinsic mechanisms.
  • TIGIT acts as an immunosuppressive molecule, regulating T cell responses relevant to autoimmune disease.