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The relationship between the cluster of differentiation 226 (CD226)/T cell Ig and ITIM domain (TIGIT) immune checkpoint and primary biliary cholangitis (PBC) pathogenesis is unknown. Herein, PBC patients ( n  = 42) showed significantly higher proportions of peripheral CD8 +  T and CD4 +  T cells expressing either CD226 or TIGIT than disease ( n  = 25) and healthy ( n  = 30) controls. The percentage of CD8 + TIGIT +  T cell was negatively associated with total bilirubin, direct bilirubin, total bile acid, γ-glutamyl transpeptidase, and alkaline phosphatase, but positively correlated with platelet count; alkaline phosphatase was positively associated with the frequency of CD8 + CD226 +  T cell; and the CD226/TIGIT ratio of CD8 +  T cell was positively associated with total bilirubin, direct bilirubin, total bile acid, γ-glutamyl transpeptidase, alkaline phosphatase, and aspartate aminotransferase to platelet ratio, but negatively correlated with albumin and platelet count. The effector function of CD8 + CD226 +  T cells was more robust than the CD8 + CD226 −  counterparts. CD226 blockade reduced CD107a + , IFN-γ + , and TNF-α +  proportions among CD8 + CD226 +  T cells, inhibiting CD8 +  T cell proliferation. In conclusion, CD226/TIGIT immune checkpoint imbalance is involved in the pathogenesis of PBC. The CD226/TIGIT ratio of CD8 +  T cell is a potential biomarker for evaluating the disease status and the prognosis of PBC patients. Moreover, CD8 + CD226 +  T cells represent a possible therapeutic target for PBC, and blocking CD226 could inhibit the activity of this cell subset  in vitro .

Imbalance of the CD226/TIGIT Immune Checkpoint Is Involved in the Pathogenesis of Primary Biliary Cholangitis