Differential expression of inhibitory receptor NKG2A distinguishes disease-specific exhausted CD8⁺ T cells.

ABSTRACT: Exhausted CD8⁺ T (Tex) cells are caused by persistent antigenic stimulation during chronic viral infection or tumorigenesis. Tex cells upregulate and sustain the expressions of multiple immune inhibitory receptors (IRs). Blocking IRs of Tex cells, exemplified by PD-1, can partially restore their effector functions and thus lead to viral suppression or tumor remission. Tex cells derived from chronic viral infections share the expression spectrum of IRs with Tex cells derived from tumors; however, whether any IRs are selectively expressed by tumor-derived Tex cells or virus-derived Tex cells remains to be learnt. In the study, we found that Tex cells upregulate IR natural killer cell lectin-like receptor isoform A (NKG2A) specifically in the context of tumor but not chronic viral

SUBMITTER: Chen X 

PROVIDER: S-EPMC8906559 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature