Table 2.

TIGIT reinforcement studies aimed at treat autoimmune diseases.

Reinforcement method	Disease	Species	Disease setting	Ref.
TIGIT-Ig fusion protein	CIA EAE	Mouse	Administration of TIGIT Vstm3 Fc-fusion protein significantly inhibited the severity of CIA and EAE	(29)
TIGIT-Ig fusion protein	SLE	Mouse	Administration of TIGIT-Ig reduced autoantibodies production and prolonged survival of SLE mice	(16)
Lentivector infection to upregulate TIGIT	CIA	Mouse	TIGIT overexpression ameliorated the severity of RA and inhibited the production of anti-collagen II antibodies	(56)
TIGIT overexpression by plasmid transfection	AA	Mouse	TIGIT overexpression on CD4+T cells alleviated disease of AA in mouse models	(127)
Agonistic anti-TIGIT Ab	MS	Human	Agonist of TIGIT showed inhibitory effects on CD4+ T cells in MS patients	(148)
Agonistic anti-TIGIT Ab	EAE	Mouse	Treatment with the agonistic anti-TIGIT Ab reduced the disease severity in EAE mouse model	(17)
Recombinant Fc-CD155	SLE	Mouse	Activation of TIGIT by recombinant CD155 protein repaired the activities of CD4+ T cells and delayed the development of SLE	(79)
Recombinant Fc-CD155	MS	Human	Activation of TIGIT signaling by Fc-CD155 represses IFN-γ production and restores the functional stability of Tregs in MS	(18)

TIGIT, T cell immunoglobulin and ITIM domain; CIA, collagen-induced arthritis; EAE, experimental autoimmune encephalomyelitis; SLE, systemic lupus erythematosus; RA, rheumatoid arthritis; AA, aplastic anemia; MS, multiple sclerosis; EAE, experimental autoimmune encephalomyelitis.