IL-17在疾病发病机制中的作用:善意的曲解。

IF 26.9 1区 医学 Q1 IMMUNOLOGY Annual review of immunology Pub Date : 2021-04-26 Epub Date: 2021-02-12 DOI:10.1146/annurev-immunol-101819-092536
Saikat Majumder, Mandy J McGeachy
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引用次数: 45

摘要

IL-17家族是一个进化古老的细胞因子家族,由6个成员(IL-17A至IL-17F)组成。IL-17家族细胞因子通过异二聚体受体发出信号,异二聚体受体包括共享的IL-17RA亚基,该亚基在全身造血细胞和非造血细胞上广泛表达。家族成员IL-17A通常被称为IL-17,因其在牛皮癣等自身免疫性疾病中的促炎作用而受到最多关注。然而,IL-17与一系列可能具有令人惊讶的可变病理的疾病有关。本文就IL-17在健康和疾病发病中的作用作一综述。为了解释IL-17在各种疾病过程中的功能,首先考虑IL-17对健康的生理功能是有用的。然后,我们讨论了这些有益的功能如何被转移到驱动慢性疾病的有害途径的致病性放大。
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IL-17 in the Pathogenesis of Disease: Good Intentions Gone Awry.

The IL-17 family is an evolutionarily old cytokine family consisting of six members (IL-17A through IL-17F). IL-17 family cytokines signal through heterodimeric receptors that include the shared IL-17RA subunit, which is widely expressed throughout the body on both hematopoietic and nonhematopoietic cells. The founding family member, IL-17A, is usually referred to as IL-17 and has received the most attention for proinflammatory roles in autoimmune diseases like psoriasis. However, IL-17 is associated with a wide array of diseases with perhaps surprisingly variable pathologies. This review focuses on recent advances in the roles of IL-17 during health and in disease pathogenesis. To decipher the functions of IL-17 in diverse disease processes it is useful to first consider the physiological functions that IL-17 contributes to health. We then discuss how these beneficial functions can be diverted toward pathogenic amplification of deleterious pathways driving chronic disease.

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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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