Abstract
Killer cell lectin-like receptor subfamily G member 1 (KLRG1) has been found on human memory T lymphocytes. However, the roles of KLRG1 on human T cells especially in tumor microenvironment have not been fully understood. Our results showed KLRG1 expression on T cells significantly increased in tumor microenvironment. KLRG1+ T cells exhibited poor proliferative capacity with decreased effector cytokine production. Meanwhile, KLRG1+ T cells expressed abundant pro-inflammatory cytokines and demonstrated high level of Foxp3 expression. KLRG1+ T cells showed decreased expression of miRNA-101 and higher expression of CtBP2. Our results indicated KLRG1 might contribute to the impaired antitumor immunity of memory T cells in tumor microenvironment. Thus, repressing KLRG1 on human memory T cells might be a novel therapeutics against cancer.
Highlights
KLRG1 is a co-inhibitory receptor belonging to inhibitory killer cell lectin-like receptors on NK cells and antigen-experienced human T cells [1, 2]
The results indicated that human T cells in tumor microenvironment expressed increased level of KLRG1
KLRG1 is considered as a senescent marker for human T cells [3]
Summary
KLRG1 is a co-inhibitory receptor belonging to inhibitory killer cell lectin-like receptors on NK cells and antigen-experienced human T cells [1, 2]. KLRG1 was thought to be a senescent marker for human T cells with poor proliferation and impaired clonal expansion after stimulation [3]. It has been reported that the expression of KLRG1 on human CD8+ T cells was elevated in the condition of virus infection, which may contribute to increased morbidity of infectious diseases [1, 4]. The expression and role of KLRG1 on human T cells in the tumor microenvironment remain to be well addressed. T-cell inhibitory receptor Tim-3 (T-cell immunoglobulin and mucin-domain containing-3) was reported to be an immune checkpoint receptor [7]. Tim-3 was considered as a surface marker for T cell exhaustion [8, 9]
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