Ye Zhi-Jian, Xu Li-Li, Zhou Qiong, Cui Ai, Wang Xiao-Juan, Zhai Kan, Wang Zhen, Tong Zhao-Hui, Shi Huan-Zhong
Department of Respiratory Medicine, First People's Hospital of Foshan, Sun Yat-sen University, Foshan, China.
Lung. 2015 Aug;193(4):539-48. doi: 10.1007/s00408-015-9738-2. Epub 2015 May 6.
The numbers of IL-27-producing CD4(+) T cells and the concentration of soluble IL-27 have been found to be increased in tuberculous pleural effusion (TPE). The objective of the present study was to explore the mechanism by which IL-27(+)CD4(+) T cells are recruited into the pleural space, and to explore the impact of IL-27 on pleural mesothelial cells (PMCs).
The expression profiles of chemokine receptor (CCR) were determined by flow cytometry. The chemoattractant activity of chemokines CCL20 and CCL22 for IL-27(+)CD4(+) T cells in vitro was observed. Effects of IL-27 on wound healing, proliferation and apoptosis of PMCs were also investigated.
IL-27(+)CD4(+) T cells in TPE expressed high level of CCR6, medium level of CCR4, and low levels of CCR2, CCR3, CCR5, CCR7, CCR10, and CXCR3. Recruitment of IL-27(+)CD4(+) T cells into TPE could be induced by pleural CCL20 and CCL22. By activating STAT3 signaling, IL-27 significantly improved wound healing and promoted proliferation of PMCs, and completely prevented apoptosis of PMCs induced by IFN-γ.
After being recruited into pleural space by CCL20 or/and CCL22, these pleural IL-27-producing CD4(+) T cells may play important roles in tuberculosis immunity by affecting PMC functions.
已发现结核性胸腔积液（TPE）中产生白细胞介素-27（IL-27）的CD4(+) T细胞数量及可溶性IL-27浓度增加。本研究的目的是探讨IL-27(+)CD4(+) T细胞被募集至胸腔的机制，并探究IL-27对胸膜间皮细胞（PMC）的影响。
通过流式细胞术测定趋化因子受体（CCR）的表达谱。观察趋化因子CCL20和CCL22在体外对IL-27(+)CD4(+) T细胞的趋化活性。还研究了IL-27对PMC伤口愈合、增殖及凋亡的影响。
TPE中的IL-27(+)CD4(+) T细胞高表达CCR6，中等表达CCR4，低表达CCR2、CCR3、CCR5、CCR7、CCR10和CXCR3。胸膜CCL20和CCL22可诱导IL-27(+)CD4(+) T细胞募集至TPE。通过激活信号转导和转录激活因子3（STAT3）信号通路，IL-27显著改善伤口愈合并促进PMC增殖，且完全阻止了γ干扰素（IFN-γ）诱导的PMC凋亡。
这些胸膜中产生IL-27的CD4(+) T细胞在被CCL20或/和CCL22募集至胸腔后，可能通过影响PMC功能在结核病免疫中发挥重要作用。
