Several pathological and inflammatory disorders induce a cytoprotective endoplasmic reticulum (ER) stress that aims at reestablishing tissue homeostasis, yet can also ignite lethal signaling pathways leading to apoptotic cell death when ER stress endures. Cells that undergo episodes of ER stress in response to pathological malfunction or cytotoxic agents can expose and release immunomodulatory damaged-associated molecular patterns (DAMPs) on their surface and into the extracellular space, respectively. Immunosuppressive DAMPs inhibit the transfer of antigens from stressed cells to antigen-presenting cells (APCs), whereas immunostimulatory DAMPs can act on APCs to facilitate antigen uptake, processing and presentation to stimulate T cell-mediated adaptive immune responses. In this review, we focus on immunomodulatory DAMPs that are released/exposed in conditions of ER stress induced in the context of chronic pathologies and anticancer therapies.

中文翻译：

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内质网应激在细胞中释放与损伤相关的分子模式。

几种病理性和炎性疾病诱发了旨在保护组织稳态的细胞保护性内质网（ER）应激，但当ER应激持续时，也可能点燃致死性信号通路，导致凋亡性细胞死亡。响应于病理性功能失常或细胞毒性剂而发生内质网应激事件的细胞可以分别在其表面和进入细胞外空间暴露并释放免疫调节受损相关分子模式（DAMP）。免疫抑制性DAMP抑制抗原从应激细胞向抗原呈递细胞（APC）的转移，而免疫刺激性DAMP可以作用于APC以促进抗原摄取，加工和呈递，从而刺激T细胞介导的适应性免疫反应。在这篇评论中