Tumors can employ different mechanisms to evade immune surveillance and function. Overexpression of co-inhibitory ligands that bind to checkpoint molecules on the surface of T-cells can greatly impair the function of latter. TIGIT (T cell immunoreceptor with Ig and ITIM domains) is such a co-inhibitory receptor expressed by T and NK cells which， upon binding to its ligand (e.g.， CD155)， can diminish cytokine production and effector function. Additionally， the absence of positive co-stimulation at the tumor site can further dampen T-cell response.
Tumors can employ different mechanisms to evade immune surveillance and function. Overexpression of co-inhibitory ligands that bind to checkpoint molecules on the surface of T-cells can greatly impair the function of latter. TIGIT (T cell immunoreceptor with Ig and ITIM domains) is such a co-inhibitory receptor expressed by T and NK cells which， upon binding to its ligand (e.g.， CD155)， can diminish cytokine production and effector function. Additionally， the absence of positive co-stimulation at the tumor site can further dampen T-cell response.
