Treg and NK cells related cytokines are associated with deep rectosigmoid endometriosis and clinical symptoms related to the disease

Microbiome Profile of Deep Endometriosis Patients: Comparison of Vaginal Fluid, Endometrium and Lesion

“…According to this theory, initially proposed by Sampson, the retrograde tubal flow seeds menstrual endometrial tissue in the peritoneal cavity and other organs, to which it adheres. However, as around 90% of women have retrograde menstruation, and just only 10% develop the disease, several authors have been proposed that other factors like anatomical, genetic, endocrine, environmental and inflammatory may influence this tissue implantation [8][9][10][11][12][13][14][15][16].…”

“…Several studies have already demonstrated, for example, that the peritoneal fluid of women with endometriosis has high levels of pro-inflammatory cytokines and growth factors, such as TNF-α, IL-1 and IL-6. In previous studies carried out by our Diagnostics 2020, 10, 163 2 of 11 research group, we described the role of inflammatory factors presented in peritoneal fluid in the immune balance of patients with endometriosis, showing an increase in the cytokines IL-2, IL-6 and TGF-β, an increase in amyloid protein A (SAA), as well as an increase in CD4(+)CD25(high)Foxp3(+) cells, and a decrease in ICOS+Treg (T regulatory cells) and CD45RO+Treg cells in patients with the disease [10,11,14].…”

Regulatory T cells isolated from endometriotic peritoneal fluid express a different number of Toll-like receptors

“…Treg cells are a subpopulation of T cells that maintain immunological self-tolerance and homeostasis, control the suppression of excessive immune response to the host (16) and have been suggested to play a role in immune impairment observed in endometriosis disease. (7)(8)(9)(10) Toll-like receptors are transmembrane proteins located on the cell surface or on the endosome wall, responsible for inducing the expression of various host defense mechanisms. (15,17) Some studies suggested that microorganisms can be directly detected by Tregs through TLR (18,19) that can modulate the suppressive function of Tregs, (19)(20)(21)(22)(23)(24) which could supposedly be enhanced or reversed by TLR agonists.…”

“…(4,5) In view of this discrepancy, complementary theories suggest that the immune response of endometriosis patients is altered, and it fails to eliminate the ectopic endometrial implants. (6)(7)(8)(9)(10) As an example, regulatory T cells (Treg) are a subpopulation of specialized immune regulation T lymphocytes, which have been already related to the development of endometriosis. (9) Although Treg are associated with the production of anti-inflammatory cytokines, there is evidence that under inflammatory conditions, they can also express inflammatory cytokines and, when unregulated, may act to maintain the disease.…”

Co-morbidity of type 1 diabetes and endometriosis: bringing a new paradigm into focus

“…A recent review (Ahn et al 2016) presents a comprehensive description of immune-inflammation genes associated with ENDO. Interferon-γ is a key molecule in ENDO (Mier-Cabrera et al 2011, Gueuvoghlanian-Silva et al 2018 and in T1DM (Driver et al 2017, Osum et al 2018, given its regulation of Th-1 cell development in autoimmunity. Tumor necrosis factor-alpha (TNF-α) is implicated in the pathogenesis of ENDO, since its levels are increased in peritoneal fluids of ENDO women by virtue of activated peritoneal macrophages infiltrating lesions and correlate with disease severity and with size and numbers of active lesions (Birt et al 2013, Kocbek et al 2016.…”