O-030 Disturbed homeostasis of regulatory T-cells and imbalanced signal transducer and activator of transcription 5 (STAT5) in women with ovarian endometriosis

Abstract Study question Do women with endometriosis have altered cytokine signalling and regulatory T-cell (Treg) homeostasis compared to controls? Summary answer Altered homeostasis of circulating Treg cells seems to be associated with STAT5 phosphorylation, which is significantly increased in women with ovarian endometriosis compared to controls. What is known already Cytokine signaling influences homeostasis of regulatory T-cells (Treg), which play a crucial role in cell-mediated immunity and are responsible for certain immune disorders. Endometriosis is a condition associated with altered immune response to endometrial cells. While some animal studies have shown that Treg deficiency facilitates ectopic implantation of endometriosis, a recent study performed in a small number of women with endometriosis has shown the decreased proportion of a specific-activated subset of Treg cells in the endometrioma compared to controls. There is no data characterising cytokine signalling in circulating Treg subsets, which could underlie their altered homeostasis in women with endometriosis. Study design, size, duration A prospective cohort study including 14 women with endometriosis and 10 controls at a university-based tertiary care centre for endometriosis. The data were collected from August 2020 to September 2021. Serum blood samples were collected in the early follicular phase of the menstrual cycle, in women not using any hormonal treatment. Early follicular steroid hormone levels were measured. A detailed expert ultrasound examination was performed to diagnose and accurately map endometriotic lesions. Participants/materials, setting, methods We investigated signal transducer and activator of transcription (STAT) signalling in peripheral blood Treg subsets, including CD45RA+FOXP3low+ naive Tregs (nTregs). Expression of proliferation marker Ki-67 and STAT activation also in FOXP3- conventional (Tcon) CD4+T-cells was monitored, hypothesising that defects in this pathway could be associated with altered Treg/Tcon homeostasis in endometriosis. Immunophenotyping and flow cytometry methods with phospho-specific antibodies that allow analysis of basal STAT activation/phosphorylation also in rare subsets of Treg cells were used. Main results and the role of chance Among women with endometriosis, 5 had evidence of ovarian and deep infiltrating endometriosis (DIE), 5 had only ovarian endometriosis and 4 had only evidence of DIE. Groups were comparable in their clinical c