Macrophages in endometriosis: they came, they saw, they conquered
Date
2022
Authors
Panir, K.
Hull, M.L.
Greaves, E.
Editors
Mor, G.
Koga, K.
Koga, K.
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Book chapter
Citation
Immunology of Endometriosis: Pathogenesis and Management, 2022 / Mor, G., Koga, K. (ed./s), vol.2, Ch.2, pp.13-41
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Kavita Panir, Mary Louise Hull, and Erin Greaves
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Abstract
Macrophages mediate the initiation and resolution of inflammation. Their phenotype and function is determined by local tissue milieu and aberrant activity contributes to chronic inflammatory disorders including endometriosis. During menstruation, macrophages initiate breakdown and scarless repair of the endometrium. In endometriosis, when endometrium is translocated to the peritoneal cavity, monocytes and macrophages colonize the ectopic tissue. The intrinsic capacity for macrophages to regenerate promotes healing of ectopic endometrium and formation of endometriotic lesions. In lesions, macrophages enhance survival and proliferation of ectopic cells and promote recruitment of vascular and neural networks. We describe macrophage roles in endometriosis, and a putative model where a dynamic lesion microenvironments impact macrophage phenotype and heterogeneity. We suggest that the process of wound repair occurs aberrantly with paradoxical phases of inflammation and healing occurring simultaneously, and contributing to fibrosis in lesions. Understanding the coexistence of multiple macrophage phenotypes may allow harnessing of their therapeutic potential.
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© 2022 Elsevier Inc. All rights reserved.