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Macrophages in patients with recurrent endometrial polyps could exacerbate Th17 responses
Author(s) -
Zhu Yali,
Liu Zhihong,
Du Miaomiao,
Yi Lisha,
Gong Guifang,
Tang Xiang
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12994
Subject(s) - rar related orphan receptor gamma , monocyte , tumor necrosis factor alpha , secretion , peripheral blood mononuclear cell , medicine , endocrinology , interleukin , interleukin 17 , inflammation , immunology , downregulation and upregulation , stimulation , biology , cytokine , immune system , in vitro , foxp3 , biochemistry , gene
Summary Endometrial polyps (EPs) are outgrowths in the endometrium with unknown etiology. The fact that EPs can often recur after surgical removal suggests that EPs are not induced by random events but by continuous or recurrent processes in patients. We previously demonstrated that the risk of EP development was positively associated with overactive Th17 responses. However, the requirements of Th17 upregulation are yet unclear. Here, we recruited 26 women with symptomatic EP and 24 without EP, and peripheral mononuclear cells were harvested for the examination of circulating immunity. Compared to controls without EP, the patients with symptomatic EP presented significantly elevated levels of monocyte activation. The circulating monocytes from patients secreted higher levels of tumor necrosis factor (TNF), interleukin (IL)‐1β, IL‐6 and IL‐23 directly ex vivo and with LPS stimulation. In memory CD4 + T cells, monocytes were not required for IL‐17 expression, but the presence of activated monocytes significantly increased the secretion of IL‐17. In naive CD4 + T cells, activated monocytes were required for significant IL‐17 secretion and RORC transcription. Interestingly, the monocytes from EP individuals were significantly more potent in promoting Th17 differentiation from naive CD4 + T cells than the monocytes from controls. Furthermore, we showed that monocyte‐mediated Th17 differentiation required the secretion of TNF, IL‐1β and IL‐6. Together, this study demonstrated activated monocytes supported Th17 inflammation in patients with EP.