Th2细胞在健康和疾病中的作用。

IF 26.9 1区 医学 Q1 IMMUNOLOGY
T. Nakayama, K. Hirahara, A. Onodera, Yusuke Endo, H. Hosokawa, K. Shinoda, D. Tumes, Y. Okamoto
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引用次数: 240

摘要

辅助T(Th)细胞亚群通过产生标志性细胞因子来指导免疫反应。Th2细胞产生IL-4、IL-5和IL-13,它们在体液免疫和保护免受蠕虫感染方面很重要,并且是许多过敏性炎症疾病的发病机制的核心。Th2细胞分化和功能维持的分子分析导致了最近的发现,这些发现完善了我们对Th2细胞生物学的理解。染色质重塑复合物如Polycomb和Trithorax对Gata3表达的表观遗传学调控对于维持Th2细胞的同一性至关重要。在过敏性疾病的背景下,已经在小鼠和人类中鉴定出记忆型致病性Th2细胞。为了更好地了解这些疾病驱动的细胞群体,我们开发了一种称为致病性Th群体疾病诱导模型的模型。确定致病性Th细胞亚群的概念可能会刺激治疗顽固性慢性炎症性疾病的新的、有效的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Th2 Cells in Health and Disease.
Helper T (Th) cell subsets direct immune responses by producing signature cytokines. Th2 cells produce IL-4, IL-5, and IL-13, which are important in humoral immunity and protection from helminth infection and are central to the pathogenesis of many allergic inflammatory diseases. Molecular analysis of Th2 cell differentiation and maintenance of function has led to recent discoveries that have refined our understanding of Th2 cell biology. Epigenetic regulation of Gata3 expression by chromatin remodeling complexes such as Polycomb and Trithorax is crucial for maintaining Th2 cell identity. In the context of allergic diseases, memory-type pathogenic Th2 cells have been identified in both mice and humans. To better understand these disease-driving cell populations, we have developed a model called the pathogenic Th population disease induction model. The concept of defined subsets of pathogenic Th cells may spur new, effective strategies for treating intractable chronic inflammatory disorders.
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来源期刊
Annual review of immunology
Annual review of immunology 医学-免疫学
CiteScore
57.20
自引率
0.70%
发文量
29
期刊介绍: The Annual Review of Immunology, in publication since 1983, focuses on basic immune mechanisms and molecular basis of immune diseases in humans. Topics include innate and adaptive immunity; immune cell development and differentiation; immune control of pathogens (viruses, bacteria, parasites) and cancer; and human immunodeficiency and autoimmune diseases. The current volume of this journal has been converted from gated to open access through Annual Reviews' Subscribe to Open program, with all articles published under a CC BY license.
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