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Projekt Druckansicht

Verbesserungen der antitumoralen CD8+ T Zellfunktion durch die Inhibierung von CD36

Fachliche Zuordnung Immunologie
Förderung Förderung von 2019 bis 2022
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 420112816
 
Erstellungsjahr 2023

Zusammenfassung der Projektergebnisse

My group identified a protein molecule, CD36, which inhibits protective immune responses in tumor. Metabolic fitness of T cells plays a pivotal role in regulating T cell-mediated immunity, and metabolic deregulation causes T cell exhaustion in chronic viral infection and cancer. The scavenger receptor CD36 limited lipid peroxidation by anti-tumor T cell-dependent immune responses. T cells adapted to alter lipid homeostasis in the tumor microenvironment by enhancing uptake and accumulation of lipids and lipid peroxidation in murine tumors. Functionally exhausted CD8+ TILs substantially increased CD36 expression, which positively correlated with lipid uptake and storage levels. In murine melanoma models, CD36-deficient T cells had considerably more robust anti-tumor activity and cytokine production than wild-type cells. These findings suggest that CD36 promotes the uptake of oxidized low-density lipoproteins (oxLDL) and induces lipid peroxidation in T cells, and oxLDL inhibits T cell functions in a CD36-dependent manner. Glutathione peroxidase 4 over-expression lowers lipid peroxidation and restores functionalities in T cells. These results suggest a critical role for the oxLDL-CD36 axis in promoting intratumoral T cell dysfunction and reveal CD36 as an immune checkpoint molecule in cancer.

Projektbezogene Publikationen (Auswahl)

 
 

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