Literature DB >> 24410406

Interplay of Th1 and Th17 cells in murine models of malignant pleural effusion.

Hua Lin1, Zhao-Hui Tong, Qian-Qian Xu, Xiu-Zhi Wu, Xiao-Juan Wang, Xiao-Guang Jin, Wan-Li Ma, Xiang Cheng, Qiong Zhou, Huan-Zhong Shi.   

Abstract

RATIONALE: IFN-γ-producing CD4(+) T (Th1) cells and IL-17-producing CD4(+) T (Th17) cells have been found to be involved in multiple malignancies; however, the reciprocal relationship between Th1 and Th17 cells in malignant pleural effusion (MPE) remains to be elucidated.
OBJECTIVES: To explore the differentiation and immune regulation of Th1 and Th17 cells in the development of MPE in murine models.
METHODS: The distribution and differentiation of Th1 and Th17 cells in MPE were investigated in IFN-γ(-/-), IL-17(-/-), and wild-type mice. The effects of Th1 and Th17 cells on the development of MPE and the survival of mice bearing MPE were also investigated.
MEASUREMENTS AND MAIN RESULTS: We have demonstrated that increased Th1 and Th17 cells could be found in MPE as compared with blood and spleen. Compared with wild-type mice, Th17 cells were markedly augmented in MPE from IFN-γ(-/-) mice, and improved survival could be seen in IFN-γ(-/-) mice. Th1 cell numbers were elevated in MPE from IL-17(-/-) mice, and decreased survival could be seen in IL-17(-/-) mice. The in vitro experiments showed that IFN-γ deficiency promoted Th17-cell differentiation by suppressing the STAT3 pathway and that IL-17 deficiency promoted Th1-cell differentiation by suppressing the STAT1 pathway.
CONCLUSIONS: In mouse models of MPE, IFN-γ inhibited Th17-cell differentiation, whereas IL-17 inhibited Th1-cell differentiation. IL-17 inhibited the formation of MPE and improved the survival of mice bearing MPE; in contrast, IFN-γ promoted MPE formation and mouse death.

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Year:  2014        PMID: 24410406     DOI: 10.1164/rccm.201310-1776OC

Source DB:  PubMed          Journal:  Am J Respir Crit Care Med        ISSN: 1073-449X            Impact factor:   21.405


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