Targeting metabolic circuitry to supercharge CD8+ T cell antitumor responses

Qiang Cai; Yihao Tian; Quazi T H Shubhra

doi:10.1016/j.cmet.2024.04.007

Targeting metabolic circuitry to supercharge CD8⁺ T cell antitumor responses

Cell Metab. 2024 May 7;36(5):884-886. doi: 10.1016/j.cmet.2024.04.007.

Authors

Qiang Cai¹, Yihao Tian², Quazi T H Shubhra³

Affiliations

¹ Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan 430060, China. Electronic address: cqno@sina.com.
² Department of Human Anatomy and Histology and Embryology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
³ Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan 430060, China; Institute of Chemistry, University of Silesia in Katowice, Szkolna 9, 40-003 Katowice, Poland. Electronic address: shubhro.du@gmail.com.

PMID: 38718753
DOI: 10.1016/j.cmet.2024.04.007

Abstract

Tumors compromise T cell functionality through various mechanisms, including the induction of a nutrient-scarce microenvironment, leading to lipid accumulation and metabolic reprogramming. Hunt et al. elucidate acetyl-CoA carboxylase's crucial role in regulating lipid metabolism in CD8⁺ T cells, uncovering a novel metabolic strategy to potentiate antitumor immune responses.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Acetyl-CoA Carboxylase* / metabolism
Animals
CD8-Positive T-Lymphocytes* / immunology
CD8-Positive T-Lymphocytes* / metabolism
Humans
Lipid Metabolism
Neoplasms / immunology
Neoplasms / metabolism
Tumor Microenvironment / immunology

Substances

Acetyl-CoA Carboxylase