KRAS-elicited PDIA6 blocks PERK-dependent immunogenic cell death in pancreatic carcinoma.

IF 6.2 2区医学 Q1 IMMUNOLOGY

Oncoimmunology Pub Date : 2026-12-31 Epub Date: 2026-03-08 DOI:10.1080/2162402X.2026.2641424

Liwei Zhao, Peng Liu, Guido Kroemer, Oliver Kepp

引用次数: 0

Abstract

KRAS-mutant pancreatic ductal adenocarcinoma (PDAC) remains largely refractory to immune checkpoint blockade. Wang et al. identified PDIA6 as a KRAS-driven suppressor of PERK-dependent immunogenic cell death, fostering immune exclusion. PDIA6 inhibition restores CD8⁺ T-cell immunity and sensitizes PDAC to immunotherapy, highlighting a targetable resistance mechanism in KRAS-mutant PDAC.

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kras诱导的PDIA6阻断胰腺癌中perk依赖性免疫原性细胞死亡。

kras突变型胰腺导管腺癌（PDAC）对免疫检查点阻断仍然有很大的难治性。Wang等人发现PDIA6是kras驱动的perk依赖性免疫原性细胞死亡抑制因子，促进免疫排斥。PDIA6抑制恢复CD8+ t细胞免疫并使PDAC对免疫治疗敏感，突出了kras突变PDAC的靶向耐药机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oncoimmunology ONCOLOGYIMMUNOLOGY-IMMUNOLOGY

CiteScore

12.50

自引率

2.80%

发文量

276

审稿时长

24 weeks

期刊介绍： OncoImmunology is a dynamic, high-profile, open access journal that comprehensively covers tumor immunology and immunotherapy. As cancer immunotherapy advances, OncoImmunology is committed to publishing top-tier research encompassing all facets of basic and applied tumor immunology. The journal covers a wide range of topics, including: -Basic and translational studies in immunology of both solid and hematological malignancies -Inflammation, innate and acquired immune responses against cancer -Mechanisms of cancer immunoediting and immune evasion -Modern immunotherapies, including immunomodulators, immune checkpoint inhibitors, T-cell, NK-cell, and macrophage engagers, and CAR T cells -Immunological effects of conventional anticancer therapies.