自身免疫和癌症免疫之间的引人入胜的科学关系，传统上被认为是突显新的病理靶点。可以理解的是，这些“慢性致命”的疾病在免疫谱的两个极端。然而，自身免疫和癌症之间的免疫调节机制并不总是相互矛盾的，有时也会根据疾病阶段、部位和时间点相互呼应。此外，针对解除免疫检查点分子或信号通路的阻断，以释放免疫反应对抗癌症的方法，正被利用来保持自身耐受性并治疗许多自身免疫性疾病。因此，理解癌症中所涉及的共同关键因素对于描绘自身免疫疾病谱并验证新的药物候选物至关重要。在本综述中，我们将广泛描述ZEB1（Zinc-finger E-box Binding Homeobox 1）在癌症中强化免疫耗竭或在自身免疫条件下造成自身耐受性丧失的作用。我们努力交流有关分子通路和病理反应（免疫调节、细胞增殖、衰老、自噬、缺氧和昼夜节律）的信息，这些过程可以通过ZEB1在自身免疫的背景下调控。这将有助于解开ZEB1复杂而紧密的发病机制，这一机制在自身免疫方面的研究相对较少，与其相对应的癌症。本综述还将进一步考虑针对自身免疫中的ZEB1的几种方法。版权所有 © 2023 Elsevier Inc. 保留所有权利。

The intriguing scientific relationship between autoimmunity and cancer immunology, have been traditionally indulged to throw spotlight on novel pathological targets. Understandably, these "slowly killing" diseases are on the opposite ends of the immune spectrum. However, the immune regulatory mechanisms between autoimmunity and cancer are not always contradictory and sometimes mirror each other based on disease stage, location, and timepoint. Moreover, the blockade of immune checkpoint molecules or signalling pathways that unleashes the immune response against cancer is being leveraged to preserve self-tolerance and treat many autoimmune disorders. Therefore, understanding the common crucial factors involved in cancer is of paramount importance to paint the autoimmune disease spectrum and validate novel drug candidates. In the current review, we will broadly describe how ZEB1, or Zinc-finger E-box Binding Homeobox 1, reinforces immune exhaustion in cancer or contributes to loss of self-tolerance in auto-immune conditions. We made an effort to exchange information about the molecular pathways and pathological responses (immune regulation, cell proliferation, senescence, autophagy, hypoxia, and circadian rhythm) that can be regulated by ZEB1 in the context of autoimmunity. This will help untwine the intricate and closely postured pathogenesis of ZEB1, that is less explored from the perspective of autoimmunity than its counterpart, cancer. This review will further consider several approaches for targeting ZEB1 in autoimmunity.Copyright © 2023 Elsevier Inc. All rights reserved.