IL-25: A key requirement for the regulation of type-2 immunity

IL-25: A key requirement for the regulation of type-2 immunity
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DOI:
10.1002/biof.24
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发表时间:
2009-03-01
期刊:
影响因子:
6
通讯作者:
McKenzie, Andrew N. J.
McKenzie, Andrew N. J.
中科院分区:
生物学2区
文献类型:
--
作者:
Barlow, Jillian L.;McKenzie, Andrew N. J.

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已经证实,以嗜酸性粒细胞增多、杯状细胞增生、粘液产生和B细胞类别转换为IgE为特征的2型免疫高度依赖于T辅助2 (Th2)细胞产生的2型细胞因子,白细胞介素(IL)-4、IL-5、IL-9和IL-13。然而,目前尚不清楚2型细胞因子效应反应是如何被诱导的,以及什么先天细胞类型会产生启动因子。最近的报道强调IL-25是一种2型诱导因子,IL-25的使用导致严重的肠道和肺部2型病变。IL-25的表达对于启动强有力的2型反应也是必要的,无论是在反应发生时,如蠕虫感染,还是在反应过程中,如实验性过敏性哮喘。同样明显的是,除了通过IL-4、IL-5和IL-13直接控制2型免疫外,IL-25还可能与其他细胞因子及其受体相互作用,如IL-17A和IL-17RA受体。在这里,我们回顾了IL-25作为控制2型反应起始和严重程度的重要因素的作用,以及作为2型细胞因子家族的替代治疗靶点,用于治疗过敏性哮喘。(C) 2009国际生物化学与分子生物学联合会第35卷,第2号;2009年3 / 4月,第178-182页。电子邮件:anm@mrc-lmb.cam.ac.uk
It has been well-established that type-2 immunity, characterized by eosinophilia, goblet cell hyperplasia, mucus production, and B cell class switching to IgE, is highly dependent on the production of the type-2 cytokines, interleukin (IL)-4, IL-5, IL-9, and IL-13, by T helper 2 (Th2) cells. However, it is less clear how the type-2 cytokine effector response is induced and in addition what innate cell type produces the initiating factor. Recent reports highlight IL-25 as a type-2 inducing factor, with IL-25 administration resulting in severe gut and lung type-2 pathologies. The expression of IL-25 is also necessary for initiation of a robust type-2 response both at the genesis of the response, as with helminth infection, and during the response, as has been shown in experimental allergic asthma. It is also apparent that, as well as directly controlling type-2 immunity via IL-4, IL-5, and IL-13, IL-25 may also interact with other cytokines and their receptors, a such as IL-17A and the IL-17RA receptor. Here, we review the role of IL-25 as an important factor in controlling the initiation and severity of the type-2 response, and as an alternative therapeutic target to the type-2 cytokine family, for the treatment of allergic asthma. (C) 2009 International Union of Biochemistry and Molecular Biology, Inc. Volume 35, Number 2; March/April 2009, Pages 178-182 . E-mail: anm@mrc-lmb.cam.ac.uk