TOX promotes the exhaustion of antitumor CD8+ T cells by preventing PD1 degradation in hepatocellular carcinoma

Compromised antitumor immunity characterized by presence of dysfunctional CD8+ T cells in the tumor microenvironment (TME) is a hallmark of cancer [1,2]. Long-term persistence of tumor antigens and/or the suppressive TME drive the progression of antitumor effector CD8+ T cells into a functionally impaired state called ‘T cell exhaustion’ [3]. Exhausted CD8+ T cells possess diminished effector functions and a distinct transcriptional profile relative to those of effector cells, and they express high amounts of inhibitory receptors, such as programmed cell death-1 (PD1), T-cell immunoglobulin and mucin-domain c ontaining-3 (TIM3), lymphocyte-activation gene 3 (LAG3) and cytotoxic T lymphocyte-associated antigen-4 (CTLA4).
Source: Journal of Hepatology - Category: Gastroenterology Authors: Source Type: research