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. 2022 Jun 24;13:914406. doi: 10.3389/fimmu.2022.914406

Table 2.

CD226 axis receptor ICD mutational studies and associated functional effects.

Receptor System (cell type) Modifications Finding(s) Ref.
CD226 (human) BW5147 (T cell line, mouse), human CD226 ectopic S329F mutation; various truncations of intracellular domain Prevention of protein kinase C (PKC) phosphorylation and subsequent cellular adhesion (31)
CD226 (human) Jurkat and NKL (T and NK cell lines, human) WT in NKL cells. Mutation of S329F in Jurkat cells S329F mutant failed to associate with LFA-1 (32)
CD226 (human) Jurkat (T cell line, human) and COS-7 (fibroblast line, monkey) Y322F Fyn induced phosphorylation at Y322, abrogated by Y322F mutation. (32)
CD226 (mouse) Primary murine NK cells and YTS (human NK cell line) Ectopic expression of mouse CD226 in YTS cells Increased phosphorylation of Erk and Akt, as well as calcium flux and target cell lysis following CD226 engagement (30)
CD226 (mouse) YTS (NK cell line, human) and transgenic mice Y319F, S326A Y319F modification in CD226 attenuated mouse NK cell cytotoxicity and IFNg production (30)
CD226 (mouse) Synthetic peptide corresponding to 315-333 of mouse CD226 Synthesized with phosphorylation at Y319, D321Q Phosphorylation of the amino acid corresponding to Y319 led to capture of Grb2. Mutation of the asparagine at +2 position led to loss of Grb2 binding (30)
CD226 (human) Jurkat (T cell line, human) or primary (T cells, human) Y322A, S329A Y322A modification, but not S329A, reduced downstream CD226 signaling after incubation with CHO-OKT3-PVR cells (33)
TIGIT (human) Jurkat (T cell line, human) Y225A, Y231A Y225A/Y231A dual mutation rescued CD69 expression on Jurkat cells following exposure to superantigen and CD155 (33)
TIGIT (human) YTS (NK cell line, human) Truncation (Y231stop); Y231A Rescue of CD155-TIGIT induced inhibition of YTS (NK) mediated cytotoxicity following truncation or Y231A mutation in TIGIT (10)
TIGIT (human) YTS (NK cell line, human) Y225A, Y231A CD155 induced TIGIT phosphorylation. Pervanadate treatment-induced phosphorylation of TIGIT was prevented with Y225A or Y225A/Y231A, but not Y231A alone (34)
TIGIT (human) YTS (NK cell line, human) Y225A, Y231A TIGIT Y225 associates with Grb2, leading to downstream inhibitory function. Nominal rescue of cytotoxicity with Y231A mutation (34)
TIGIT (human) YTS (NK cell line, human) Y225A, Y231A Reduced association with β-arrestin 2 following mutation Y225A or Y225A/Y231A, but not Y231A alone (35)
TIGIT (human) Jurkat (T cell line, human) ICD truncation, Y225F, Y231F TIGIT intracellular domain is not required to prevent PVR-induced CD226 phosphorylation (36)
TIGIT (human) Cell-free liposome ICD expressed on cell-free liposome Lack of Shp2, Shp1, Zap70, Grb2, SHIP-1, or P50a recruitment following phosphorylation of TIGIT ICD by Fyn (36)
CD96 Undescribed Undescribed Undescribed None
PVRIG (human) HEK293T (kidney cell line, human) and MOLT4 (T cell line, human) Y233F, Y293F Y233F mutation reduced phosphorylation after pervanadate treatment. PVRIG associates with SHIP and Shp1/2 following pervanadate treatment (9)