肥胖中的免疫失调。

IF 28.4 1区 医学 Q1 PATHOLOGY
Zewen Jiang, Chihiro Tabuchi, Sarah G Gayer, Sagar P Bapat
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引用次数: 0

摘要

免疫系统在维持生理稳态中起着重要作用。随着肥胖(一种以慢性炎症和全身失衡为特征的状态)的日益流行,科学和临床对肥胖如何重塑免疫功能的了解越来越感兴趣。在这篇综述中,我们提出肥胖不仅是一种代谢状态的改变,也是一种从根本上改变的免疫状态。我们总结了关键的开创性和最近的发现,阐明了肥胖如何影响免疫功能,包括其在微生物防御中的经典作用,它对哮喘等适应性不良炎症疾病的贡献,以及它对抗肿瘤免疫的影响。我们还探讨了肥胖如何调节组织实质内的免疫功能,特别关注T细胞在脂肪组织中的作用。最后,我们考虑了未来的研究领域,包括体重减轻后肥胖对免疫功能的持久影响,例如使用胰高血糖素样肽-1 (GLP-1)受体激动剂治疗的结果。总之,这篇综述强调了全身代谢在塑造免疫细胞功能中的关键作用,对各种生理环境下的组织稳态具有深远的意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immune Dysregulation in Obesity.

The immune system plays fundamental roles in maintaining physiological homeostasis. With the increasing prevalence of obesity-a state characterized by chronic inflammation and systemic dyshomeostasis-there is growing scientific and clinical interest in understanding how obesity reshapes immune function. In this review, we propose that obesity is not merely an altered metabolic state but also a fundamentally altered immunological state. We summarize key seminal and recent findings that elucidate how obesity influences immune function, spanning its classical role in microbial defense, its contribution to maladaptive inflammatory diseases such as asthma, and its impact on antitumor immunity. We also explore how obesity modulates immune function within tissue parenchyma, with a particular focus on the role of T cells in adipose tissue. Finally, we consider areas for future research, including investigation of the durable aspects of obesity on immunological function even after weight loss, such as those observed with glucagon-like peptide-1 (GLP-1) receptor agonist treatment. Altogether, this review emphasizes the critical role of systemic metabolism in shaping immune cell functions, with profound implications for tissue homeostasis across various physiological contexts.

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来源期刊
CiteScore
62.60
自引率
0.00%
发文量
40
期刊介绍: The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.
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