Ye Zhi-Jian, Zhou Qiong, Du Rong-Hui, Li Xiao, Huang Bo, Shi Huan-Zhong
Department of Respiratory Diseases, Key Laboratory of Pulmonary Diseases of Health Ministry, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Clin Vaccine Immunol. 2011 Oct;18(10):1608-15. doi: 10.1128/CVI.05214-11. Epub 2011 Aug 3.
Both T helper interleukin 17 (IL-17)-producing cells (Th17 cells) and regulatory T cells (Tregs) have been found to be increased in human tuberculous pleural effusion (TPE); however, the possible interaction between Th17 cells and Tregs in TPE remains to be elucidated. The objective of the present study was to investigate the distribution of Th17 cells in relation to Tregs, as well as the mechanism of Tregs in regulating generation and differentiation of Th17 cells in TPE. In the present study, the numbers of Th17 cells and Tregs in TPE and blood were determined by flow cytometry. The regulation and mechanism of CD39(+) Tregs on generation and differentiation of Th17 cells were explored. Our data demonstrated that the numbers of Th17 cells and CD39(+) Tregs were both increased in TPE compared with blood. Th17 cell numbers were correlated negatively with Tregs in TPE but not in blood. When naïve CD4(+) T cells were cultured with CD39(+) Tregs, Th17 cell numbers decreased as CD39(+) Treg numbers increased, and the addition of the anti-latency-associated peptide monoclonal antibody to the coculture reversed the inhibitory effect exerted by CD39(+) Tregs. This study shows that Th17/Treg imbalance exists in TPE and that pleural CD39(+) Tregs inhibit generation and differentiation of Th17 cells via a latency-associated peptide-dependent mechanism.
已发现,在人类结核性胸腔积液(TPE)中,产生辅助性T细胞白细胞介素17(IL-17)的细胞(Th17细胞)和调节性T细胞(Tregs)均增多;然而,TPE中Th17细胞与Tregs之间可能存在的相互作用仍有待阐明。本研究的目的是探讨Th17细胞与Tregs相关的分布情况,以及Tregs在TPE中调节Th17细胞生成和分化的机制。在本研究中,采用流式细胞术测定TPE和血液中Th17细胞和Tregs的数量。探讨了CD39(+) Tregs对Th17细胞生成和分化的调节作用及其机制。我们的数据表明,与血液相比,TPE中Th17细胞和CD39(+) Tregs的数量均增加。TPE中Th17细胞数量与Tregs呈负相关,而血液中则无此相关性。当用CD39(+) Tregs培养初始CD4(+) T细胞时,Th17细胞数量随CD39(+) Treg数量增加而减少,向共培养体系中添加抗潜伏相关肽单克隆抗体可逆转CD39(+) Tregs的抑制作用。本研究表明,TPE中存在Th17/Treg失衡,并且胸膜CD39(+) Tregs通过潜伏相关肽依赖性机制抑制Th17细胞的生成和分化。