抗pd -1治疗的耐药性是由CD30+调节性T细胞活性驱动的

IF 27.7 1区医学 Q1 IMMUNOLOGY

Nature Immunology Pub Date : 2025-06-10 DOI:10.1038/s41590-025-02175-x

引用次数: 0

摘要

我们发现PD-1的缺失增强了肿瘤微环境中调节性T （Treg）细胞的免疫抑制功能。这种增加的Treg细胞功能是由于pd -1缺陷Treg细胞上CD30驱动的共抑制受体网络的上调。阻断CD30可逆转Treg细胞介导的肿瘤生长促进。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Resistance to anti-PD-1 therapy is driven by CD30+ regulatory T cell activity

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Resistance to anti-PD-1 therapy is driven by CD30+ regulatory T cell activity

We show that deletion of PD-1 enhances regulatory T (Treg) cell immunosuppressive function in the tumor microenvironment. This increased Treg cell function results from upregulation of a co-inhibitory receptor network driven by CD30 on PD-1-deficient Treg cells. Blocking CD30 reverses Treg cell-mediated promotion of tumor growth.

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来源期刊

Nature Immunology 医学-免疫学

CiteScore

40.00

自引率

2.30%

发文量

248

审稿时长

4-8 weeks

期刊介绍： Nature Immunology is a monthly journal that publishes the highest quality research in all areas of immunology. The editorial decisions are made by a team of full-time professional editors. The journal prioritizes work that provides translational and/or fundamental insight into the workings of the immune system. It covers a wide range of topics including innate immunity and inflammation, development, immune receptors, signaling and apoptosis, antigen presentation, gene regulation and recombination, cellular and systemic immunity, vaccines, immune tolerance, autoimmunity, tumor immunology, and microbial immunopathology. In addition to publishing significant original research, Nature Immunology also includes comments, News and Views, research highlights, matters arising from readers, and reviews of the literature. The journal serves as a major conduit of top-quality information for the immunology community.