The enrichment of Arg1+ILC2s and ILCregs facilitates the progression of endometriosis: A preliminary study
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This study investigated the role of Arg1+ILC2s and ILCregs in endometriosis progression, finding their enrichment contributes to disease advancement.
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Abstract
Innate lymphoid cells (ILCs) are a kind of lymphocytes that reside in the tissue and have an essential function in the immune microenvironment. However, the relationship between endometriosis (EMS) and ILCs is complex and not fully understood. This study examines several groups of ILCs in the peripheral blood (PB), peritoneal fluid (PF) and endometrium of patients with EMS via flow cytometry. The study observed an increase in PB ILCs, particularly ILC2s and ILCregs subsets and Arg1+ILC2s in the EMS patients were highly activated. EMS patients had significantly higher levels of serum interleukin (IL)-10/33/25 compared to controls. We also found an elevation of Arg1+ILC2s in the PF and higher levels of ILC2s and ILCregs in ectopic endometrium compared with eutopic. Importantly, a positive correlation was observed between the enrichment of Arg1+ILC2s and ILCregs in the PB of EMS patients. The findings indicate that the involvement of Arg1+ILC2s and ILCregs fosters potentially endometriosis progression.
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References (43)
- CD33<sup>+</sup>CD14<sup>+</sup>CD11b<sup>+</sup>HLA‐DR<sup>−</sup> monocytic myeloid‐derived suppressor cells recruited and activated by CCR9/CCL25 are crucial for the pathogenic progression of endometriosis via openalex
- Consensus on current management of endometriosis via openalex
- Endometriosis via openalex
- Endometriosis via openalex
- Endometriosis: pathogenesis and treatment via openalex
- Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis via openalex
- The link between immunity, autoimmunity and endometriosis: a literature update via openalex
- Treg and NK cells related cytokines are associated with deep rectosigmoid endometriosis and clinical symptoms related to the disease via openalex
- W2086722297 via openalex
- W2136221987 via openalex
- W2318250120 via openalex
- W2323768961 via openalex
- W2343795401 via openalex
- W2344776862 via openalex
- W2466946637 via openalex
- W2467696249 via openalex
- W2623394978 via openalex
- W2746722198 via openalex
- W2747461977 via openalex
- W2797582001 via openalex
- W2884952568 via openalex
- W2888376450 via openalex
- W2902702934 via openalex
- W2913268586 via openalex
- W2918877774 via openalex
- W2922566219 via openalex
- W2941959759 via openalex
- W2945534157 via openalex
- W3005525322 via openalex
- W3008157654 via openalex
- W3021916818 via openalex
- W3202873424 via openalex
- W3208517554 via openalex
- W4205104064 via openalex
- W4229062835 via openalex
- W3165294846 via openalex
- W1595949461 via openalex
- W1608909099 via openalex
- W1995070836 via openalex
- W2024183493 via openalex
- W2033289727 via openalex
- W2051465794 via openalex
- W2082554712 via openalex
Cited by (2)
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- europepmc
- last seen: 2026-08-04T06:16:37.499272+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-08-04T06:15:45.464366+00:00
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