CSF-1-induced DC-SIGN + macrophages are present in the ovarian endometriosis

Researchers have found that macrophages are the predominant cells in the peritoneal fluid (PF) of endometriosis patients. CSF-1 has been found to accumulate in the lesions and PF of endometriosis patients, and CSF-1 induces THP-1-derived macrophages to polarize toward a CD169 DC-SIGN phenotype. Does...

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Published inReproductive biology and endocrinology Vol. 20; no. 1; p. 48
Main Authors Xiaocui, Li, Wei, Hong, Yunlang, Cai, Zhenzhen, Zheng, Min, An
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 08.03.2022
BioMed Central
BMC
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Summary:Researchers have found that macrophages are the predominant cells in the peritoneal fluid (PF) of endometriosis patients. CSF-1 has been found to accumulate in the lesions and PF of endometriosis patients, and CSF-1 induces THP-1-derived macrophages to polarize toward a CD169 DC-SIGN phenotype. Does the cytokine CSF-1 induce monocytes to differentiate into macrophages with a DC-SIGN phenotype in endometriosis? The level of CSF-1 in the endometrium of control subjects, and the eutopic, and ectopic endometrium of endometriosis patients was evaluated by real-time polymerase chain reaction (qRT-PCR) and was determined by enzyme-linked immunosorbent assay (ELISA) in the PF of control and endometriosis patients. CSF-1 expression was examined with a MILLIPLEX MAP Mouse Cytokine/Chemokine Magnetic Bead Panel. DC-SIGN macrophages were detected by immunohistochemical staining of tissues and flow cytometric analysis of the PF of control subjects (N = 25) and endometriosis (N = 35) patients. The phenotypes and biological activities of CSF-1 -induced macrophages were compared in an in vitro coculture system with peripheral blood lymphocytes from control subjects. In this study, we found that the proportion of DC-SIGN CD169 macrophages was higher in the abdominal immune microenvironment of endometriosis patients. CSF-1 was primarily secreted from ectopic lesions and peritoneum in mice with endometriosis. In addition, CSF-1 induced the polarization of macrophages toward a DC-SIGN CD169 phenotype; this effect was abolished by the addition of an anti-CSF-1R antibody. CSF-1 induced the generation of DC-SIGN macrophages, leading to a depressed status of peripheral blood lymphocytes, including a high percentage of Treg cells and a low percentage of CD8 T cells. Similarly, blockade with the anti-CSF-1R antibody abrogated this biological effect. This is the first study on the role of DC-SIGN macrophages in the immune microenvironment of endometriosis. Further study of the mechanism and biological activities of CSF-1-induced DC-SIGN macrophages will enhance our understanding of the physiology of endometriosis.
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ISSN:1477-7827
1477-7827
DOI:10.1186/s12958-022-00901-w