Mononuclear Phagocyte Biology
Epigenetics of Cell Differentiation

Journal Club

Zellbiologisches Literaturseminar für Doktoranden (Vst. Nr. 56265)
Thursday 9:00 am, biweekly
in D53.320 (LIT seminar room) and via Zoom


next date: 23.06.2022
CD36-mediated ferroptosis dampens intratumoral CD8+ T cell effector function and impairs their antitumor ability

Ma et al.

Cell Metabolism 33, 1001–1012 May 4, 2021 ª 2021 Elsevier Inc. https://doi.org/10.1016/j.cmet.2021.02.015

Understanding the mechanisms underlying how T cells become dysfunctional in a tumor microenvironment (TME) will greatly benefit cancer immunotherapy. We found that increased CD36 expression in tumor-infiltrating CD8+ T cells, which was induced by TME cholesterol, was associated with tumor progression and poor survival in human and murine cancers. Genetic ablation of Cd36 in effector CD8+ T cells exhibited increased cytotoxic cytokine production and enhanced tumor eradication. CD36 mediated uptake of fatty acids by tumor-infiltrating CD8+ T cells in TME, induced lipid peroxidation and ferroptosis, and led to reduced cytotoxic cytokine production and impaired antitumor ability. Blocking CD36 or inhibiting ferroptosis in CD8+ T cells effectively restored their antitumor activity and, more importantly, possessed greater antitumor efficacy in combination with anti-PD-1 antibodies. This study reveals a new mechanism of CD36 regulating the function of CD8+ effector T cells and therapeutic potential of targeting CD36 or inhibiting ferroptosis to restore T cell function.

Read the paper

Schedule

05.05.22 AG Poeck
19.05.22 AG Pukrop (Zoom only!)
02.06.22 AG Rehli
23.06.22 AG Kreutz
14.07.22 AG Hoffmann

last updated: 20.06.2022


Michael Rehli • Dept. Internal Medicine III • University Hospital
F.-J.-Strauss Allee 11 • 93053 Regensburg • Germany

Imprint & Privacy