Lockhart Euan, Green Angela M, Flynn JoAnne L
Department of Molecular Genetics and Biochemistry, Biomedical Science Tower, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
J Immunol. 2006 Oct 1;177(7):4662-9. doi: 10.4049/jimmunol.177.7.4662.
IL-17 is a cytokine produced by T cells in response to IL-23. Recent data support a new subset of CD4 Th cells distinct from Th1 or Th2 cells that produce IL-17 and may contribute to inflammation. In this study, we demonstrate that, in naive mice, as well as during Mycobacterium tuberculosis infection, IL-17 production is primarily from gammadelta T cells and other non-CD4(+)CD8(+) cells, rather than CD4 T cells. The production of IL-17 by these cells is stimulated by IL-23 alone, and strongly induced by the cytokines, including IL-23, produced by M. tuberculosis-infected dendritic cells. IL-23 is present in the lungs early in infection and the IL-17-producing cells, such as gammadelta T cells, may represent a central innate protective response to pulmonary infection.
白细胞介素-17(IL-17)是T细胞在白细胞介素-23(IL-23)刺激下产生的一种细胞因子。近期数据支持存在一种不同于Th1或Th2细胞的新型CD4辅助性T细胞亚群,该亚群可产生IL-17并可能促进炎症反应。在本研究中,我们证明,在未感染的小鼠以及结核分枝杆菌感染期间,IL-17主要由γδT细胞和其他非CD4(+)CD8(+)细胞产生,而非CD4 T细胞。这些细胞产生IL-17仅受IL-23刺激,且受到结核分枝杆菌感染的树突状细胞产生的包括IL-23在内的细胞因子的强烈诱导。IL-23在感染早期即存在于肺部,产生IL-17的细胞,如γδT细胞,可能代表对肺部感染的一种关键先天性保护反应。