Targeting T cell mitochondrial metabolism loss for antitumor immunity

Targeting T cell surface proteins that promote mitochondrial metabolism loss and T cell exhaustion in response to type I interferon or chronic ultraviolet exposure could help treat cancer by increasing antitumor immunity, and resensitizing anti-PD1 mAb-resistant tumors to immunotherapy.

Protein and mRNA expression of LY6A, a mouse T cell surface protein that promotes mitochondrial loss, were increased in CD8⁺ and CD4⁺ T cells from the skin-draining lymph nodes of mice treated with chronic ultraviolet radiation compared with those of mock irradiated mice, and LY6A expression was correlated with expression of type I interferon genes in the T cells. ...