Interleukin 23 in Crohn's disease.
Interleukin 23 in Crohn's disease.
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DOI：
10.1097/01.mib.0000442014.52661.20
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发表时间：
2014-03
影响因子：
4.9
通讯作者：
Oukka M
中科院分区：
文献类型：
--
作者：
Eken A;Singh AK;Oukka M
克罗恩病(CD)是一种终生炎症性疾病，有潜在的环境和遗传因素。CD影响胃肠道的多个部位，在西方社会的发病率越来越高。在全基因组关联研究中，IL-23受体(IL-23R)变异体已被确定为CD的易感或耐药因素。因此，IL-23在许多小鼠模型的实验性IBD的发展中是必需的。IL-23R由天然免疫细胞和获得性免疫细胞表达，包括Th17、NKT、γδT细胞和RoRγT+天然淋巴样细胞，均能在IL-23刺激下分泌IL-17A、IL-17F、IL-22和γ。在过去的十年中，这些细胞因子在IBD发病机制中的致病和保护作用已被描述。最近，先天淋巴样细胞被认为与疾病的发展有关。在这篇综述中，我们总结和讨论了这些发现，不仅强调了Th17，而且还强调了天然淋巴样细胞在疾病病因中的作用。
Crohn's Disease (CD) is a lifelong inflammatory condition with underlying environmental and genetic components. CD affects multiple parts of the gastrointestinal tract and has a growing incidence in Western societies. IL-23 receptor (IL-23R) variants have been identified as susceptibility or resistance factors for CD in genome-wide association studies. Accordingly, IL-23 is required for the development of experimental IBD in many murine models. IL-23R is expressed by both innate and adaptive immune cells which include Th17, NKT, γδ T cells and RORγT+ innate lymphoid cells all of which are capable of secreting IL-17A, IL-17F, IL-22 and IFN-γ upon IL-23 stimulation. During the last decade pathogenic and protective roles have been described for these cytokines in the IBD pathogenesis. More recently, innate lymphoid cells have been implicated in disease development. In this review, we have summarized and discussed these findings with an emphasis on not only the contribution of Th17 but also of innate lymphoid cells to disease etiology.