Emerging Functions of IL-33 in Homeostasis and Immunity.

IF 26.9 1区 医学 Q1 IMMUNOLOGY
Annual review of immunology Pub Date : 2022-04-26 Epub Date: 2022-01-05 DOI:10.1146/annurev-immunol-101320-124243
Gaelen K Dwyer, Louise M D'Cruz, Hēth R Turnquist
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引用次数: 29

Abstract

Our understanding of the functions of the IL-1 superfamily cytokine and damage-associated molecular pattern IL-33 continues to evolve with our understanding of homeostasis and immunity. The early findings that IL-33 is a potent driver of type 2 immune responses promoting parasite expulsion, but also inflammatory diseases like allergy and asthma, have been further supported. Yet, as the importance of a type 2 response in tissue repair and homeostasis has emerged, so has the fundamental importance of IL-33 to these processes. In this review, we outline an evolving understanding of IL-33 immunobiology, paying particular attention to how IL-33 directs a network of ST2+ regulatory T cells, reparative and regulatory macrophages, and type 2 innate lymphoid cells that are fundamental to tissue development, homeostasis, and repair.

IL-33在体内平衡和免疫中的新功能。
我们对IL-1超家族细胞因子和损伤相关分子模式IL-33的功能的理解随着我们对体内平衡和免疫的理解而不断发展。早期的研究发现,IL-33是促进寄生虫排出的2型免疫反应的有效驱动因素,也是过敏和哮喘等炎症性疾病的驱动因素,这一发现得到了进一步的支持。然而,随着2型反应在组织修复和体内平衡中的重要性逐渐显现,IL-33在这些过程中的基本重要性也逐渐显现。在这篇综述中,我们概述了对IL-33免疫生物学的不断发展的理解,特别关注IL-33如何指导ST2+调节性T细胞、修复性和调节性巨噬细胞以及2型先天淋巴样细胞网络,这些细胞对组织发育、稳态和修复至关重要。
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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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