IFNγ 帮助 CBLB 缺陷型 CD8+ T 细胞抵抗 Tregs。

IFNγ Helps CBLB-Deficient CD8+ T Cells to Put Up Resistance to Tregs.

机构信息

Department of Internal Medicine V, Hematology and Oncology, Comprehensive Cancer Center Innsbruck (CCCI) and Tyrolean Cancer Research Institute (TKFI), Medical University of Innsbruck, Innsbruck, Austria.

Institute of Cell Genetics, Department for Genetics, Medical University of Innsbruck, Innsbruck, Austria.

出版信息

Cancer Immunol Res. 2022 Apr 1;10(4):370. doi: 10.1158/2326-6066.CIR-22-0080.

DOI:10.1158/2326-6066.CIR-22-0080

PMID:35362047

Abstract

In this issue, Han and colleagues demonstrate in preclinical cancer models that genetic deletion of the E3 ubiquitin ligase Cbl proto-oncogene B (CBLB) in adoptively transferred CD8+ T cells induces resistance to regulatory T cells. CBLB deletion induces IFNγ and downmodulates TGFβ/SMAD signaling. This ultimately enforces these cells to be way more effective against various cancers. See related article by Han et al., p. 437 (4).

摘要

在本期中，韩等人在临床前癌症模型中证明，在过继转移的 CD8+T 细胞中遗传删除 E3 泛素连接酶原癌基因 CblB（CBLB）可诱导对调节性 T 细胞的抗性。CBLB 缺失诱导 IFNγ 并下调 TGFβ/SMAD 信号。这最终使这些细胞对各种癌症更有效。见韩等人的相关文章，第 437 页（4）。