(no title)

Chloe Hogg, Kavita Panir, Priya Dhami, Matthew Rosser, Matthias Mack, Daniel Soong, Jeffrey W. Pollard, S. Jenkins, Andrew W. Horne, Erin Greaves
2021 · W3105093764
preprint OA: green CC0 ⤵ 3 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

This study found that lesion-resident macrophages in endometriosis originate from eutopic endometrial tissue and that depleting these macrophages or promoting monocyte recruitment reduces lesion size, suggesting a role for monocyte-derived macrophages in limiting disease.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

The provided text does not include the paper’s abstract, methods, results, or discussion, only administrative/project metadata (journal, date, and affiliations). Because the substantive scientific content is missing, the key findings, study population/methods, and any explicitly stated limitations cannot be extracted or summarized reliably. The excerpt also does not mention endometriosis or adenomyosis by name in any context. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Macrophages are intimately involved in the pathophysiology of endometriosis, a chronic inflammatory disorder characterized by the growth of endometrial-like tissue (lesions) outside the uterus. By combining genetic and pharmacological monocyte and macrophage depletion strategies we determined the ontogeny and function of macrophages in a mouse model of induced endometriosis. We demonstrate that lesion-resident macrophages are derived from eutopic endometrial tissue, infiltrating large peritoneal macrophages (LpM) and monocytes. Furthermore, we found endometriosis to trigger continuous recruitment of monocytes and expansion of CCR2+ LpM. Depletion of eutopic endometrial macrophages results in smaller endometriosis lesions, whereas constitutive inhibition of monocyte recruitment significantly reduces peritoneal macrophage populations and increases the number of lesions. Reprogramming the ontogeny of peritoneal macrophages such that embryo-derived LpM are replaced by monocyte-derived LpM decreases the number of lesions that develop. We propose a putative model whereby endometrial macrophages are "proendometriosis" while newly recruited monocyte-derived macrophages, possibly in LpM form, are "antiendometriosis." These observations highlight the importance of monocyte-derived macrophages in limiting disease progression.

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Condition tags

endometriosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (54)

Cited by (3)

Source provenance

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last seen: 2026-06-10T17:14:06.276822+00:00
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