CD36-mediated metabolic adaptation supports regulatory T cell survival and function in tumors.

ABSTRACT: Depleting regulatory T cells (T_reg cells) to counteract immunosuppressive features of the tumor microenvironment (TME) is an attractive strategy for cancer treatment; however, autoimmunity due to systemic impairment of their suppressive function limits its therapeutic potential. Elucidating approaches that specifically disrupt intratumoral T_reg cells is direly needed for cancer immunotherapy. We found that CD36 was selectively upregulated in intrautumoral T_reg cells as a central metabolic modulator. CD36 fine-tuned mitochondrial fitness via peroxisome proliferator-activated receptor-β signaling, programming T_reg cells to adapt to a lactic acid-enriched TME. Genetic ablation of Cd36 in T_reg cells suppressed tumor growth accompanied by a

SUBMITTER: Wang H 

PROVIDER: S-EPMC7043937 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature