Lee Youjin, Collins Mary, Kuchroo Vijay K
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
J Clin Immunol. 2014 Jul;34 Suppl 1(0 1):S56-60. doi: 10.1007/s10875-014-0040-5. Epub 2014 May 1.
Recent findings indicate that the role of Th17 cells in the pathogenesis of tissue inflammation and autoimmunity has become rather complicated. While interleukin-17 (IL-17) producing CD4+ T cells are found frequently within the peripheral target tissue during the course of autoimmune disease, these cells may contribute to or protect from inflammation. Accumulating reports have revealed the existence of both pathogenic and non-pathogenic Th17 cells. These Th17 subsets produce the signature cytokines IL-17A and IL-17F yet have distinct and divergent roles in inducing autoimmune tissue inflammation. Comparative genomic sequence analyses between the pathogenic and non-pathogenic Th17 cells have exposed unexpected and extensive population heterogeneity within the Th17 subset. Here we review some of the unexpected factors that may drive pathogenic divergence. Understanding the functional consequences of Th17 cell diversity may allow for the selection of more precise targets for intervention in autoimmune and inflammatory diseases.
最近的研究结果表明，Th17细胞在组织炎症和自身免疫发病机制中的作用已变得相当复杂。虽然在自身免疫性疾病过程中，在外周靶组织中经常发现产生白细胞介素-17（IL-17）的CD4 + T细胞，但这些细胞可能促进炎症或起到抗炎作用。越来越多的报告揭示了致病性和非致病性Th17细胞的存在。这些Th17亚群产生标志性细胞因子IL-17A和IL-17F，但在诱导自身免疫性组织炎症中具有不同且相反的作用。致病性和非致病性Th17细胞之间的比较基因组序列分析揭示了Th17亚群中意想不到的广泛群体异质性。在此，我们综述了一些可能导致致病性差异的意外因素。了解Th17细胞多样性的功能后果可能有助于为自身免疫性和炎性疾病的干预选择更精确的靶点。
