FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4283731304> ?p ?o ?g. }

• W4283731304 abstract "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 characteristics, there was no difference in the median age of women with endometriosis and controls; 31 (range 23-45) vs. 34 (range 27-39). We demonstrated significantly higher levels of phosphorylated STAT5 (pSTAT5) in nTreg from women with ovarian endometriosis compared to controls (p = 0.026). To assess the homeostatic balance between the nTreg and Tcon, we compared pSTAT5 levels between these cell subsets in each patient. STAT5 phosphorylation was significantly higher in Tcon than in nTreg subset (p &lt; 0.001). Considering STAT5 activation in nTreg subset, this was positively correlated with the proportion of nTreg among CD4+T-cells (rs=0.54, p = 0.027) in all women with endometriosis. We also found a significant positive correlation between pSTAT5 levels in Tcon from women with endometriosis and the percentage of Ki-67+ cells in the Tcon subset (rs=0.66, p = 0.005) as well a significant correlation between luteinizing hormone (LH) levels and pSTAT5 in Tcon subset of CD4 cells (rs=0.71, p = 0.02). This implies LH-dependent imbalanced STAT5 signalling that could be responsible for increased Tcon homeostatic proliferation. Limitations, reasons for caution Our sample size is relatively small and the findings should be validated in future prospective studies. Due to the sample size, there is a risk for Type I error, although the results are coherent in indicating disturbance of Treg homeostasis. Wider implications of the findings Our study suggests that altered STAT5 signalisation may be associated with disturbed nTreg/Tcon homeostasis, which seems to be mostly prominent in women with ovarian endometriosis. If confirmed by further studies in the future, targeted treatment options could be developed to supress progress of endometriosis in this group of women. Trial registration number not applicable" @default.
• W4283731304 created "2022-07-01" @default.
• W4283731304 creator A5001936829 @default.
• W4283731304 creator A5009426351 @default.
• W4283731304 creator A5020072239 @default.
• W4283731304 creator A5022148355 @default.
• W4283731304 creator A5026983365 @default.
• W4283731304 creator A5034471200 @default.
• W4283731304 creator A5049563393 @default.
• W4283731304 date "2022-06-29" @default.
• W4283731304 modified "2023-10-18" @default.
• W4283731304 title "O-030 Disturbed homeostasis of regulatory T-cells and imbalanced signal transducer and activator of transcription 5 (STAT5) in women with ovarian endometriosis" @default.
• W4283731304 doi "https://doi.org/10.1093/humrep/deac104.030" @default.
• W4283731304 hasPublicationYear "2022" @default.
• W4283731304 type Work @default.
• W4283731304 citedByCount "0" @default.
• W4283731304 crossrefType "journal-article" @default.
• W4283731304 hasAuthorship W4283731304A5001936829 @default.
• W4283731304 hasAuthorship W4283731304A5009426351 @default.
• W4283731304 hasAuthorship W4283731304A5020072239 @default.
• W4283731304 hasAuthorship W4283731304A5022148355 @default.
• W4283731304 hasAuthorship W4283731304A5026983365 @default.
• W4283731304 hasAuthorship W4283731304A5034471200 @default.
• W4283731304 hasAuthorship W4283731304A5049563393 @default.
• W4283731304 hasBestOaLocation W42837313041 @default.
• W4283731304 hasConcept C126322002 @default.
• W4283731304 hasConcept C134018914 @default.
• W4283731304 hasConcept C170493617 @default.
• W4283731304 hasConcept C171958077 @default.
• W4283731304 hasConcept C187785154 @default.
• W4283731304 hasConcept C203014093 @default.
• W4283731304 hasConcept C2777391703 @default.
• W4283731304 hasConcept C2778690821 @default.
• W4283731304 hasConcept C2778923194 @default.
• W4283731304 hasConcept C2779306644 @default.
• W4283731304 hasConcept C2779391668 @default.
• W4283731304 hasConcept C2779522080 @default.
• W4283731304 hasConcept C3018667095 @default.
• W4283731304 hasConcept C62478195 @default.
• W4283731304 hasConcept C63645605 @default.
• W4283731304 hasConcept C71924100 @default.
• W4283731304 hasConcept C86803240 @default.
• W4283731304 hasConcept C8891405 @default.
• W4283731304 hasConcept C95444343 @default.
• W4283731304 hasConceptScore W4283731304C126322002 @default.
• W4283731304 hasConceptScore W4283731304C134018914 @default.
• W4283731304 hasConceptScore W4283731304C170493617 @default.
• W4283731304 hasConceptScore W4283731304C171958077 @default.
• W4283731304 hasConceptScore W4283731304C187785154 @default.
• W4283731304 hasConceptScore W4283731304C203014093 @default.
• W4283731304 hasConceptScore W4283731304C2777391703 @default.
• W4283731304 hasConceptScore W4283731304C2778690821 @default.
• W4283731304 hasConceptScore W4283731304C2778923194 @default.
• W4283731304 hasConceptScore W4283731304C2779306644 @default.
• W4283731304 hasConceptScore W4283731304C2779391668 @default.
• W4283731304 hasConceptScore W4283731304C2779522080 @default.
• W4283731304 hasConceptScore W4283731304C3018667095 @default.
• W4283731304 hasConceptScore W4283731304C62478195 @default.
• W4283731304 hasConceptScore W4283731304C63645605 @default.
• W4283731304 hasConceptScore W4283731304C71924100 @default.
• W4283731304 hasConceptScore W4283731304C86803240 @default.
• W4283731304 hasConceptScore W4283731304C8891405 @default.
• W4283731304 hasConceptScore W4283731304C95444343 @default.
• W4283731304 hasIssue "Supplement_1" @default.
• W4283731304 hasLocation W42837313041 @default.
• W4283731304 hasOpenAccess W4283731304 @default.
• W4283731304 hasPrimaryLocation W42837313041 @default.
• W4283731304 hasRelatedWork W1964228140 @default.
• W4283731304 hasRelatedWork W1986759961 @default.
• W4283731304 hasRelatedWork W2074673535 @default.
• W4283731304 hasRelatedWork W2091225147 @default.
• W4283731304 hasRelatedWork W2165563128 @default.
• W4283731304 hasRelatedWork W2166628562 @default.
• W4283731304 hasRelatedWork W226179855 @default.
• W4283731304 hasRelatedWork W2897315531 @default.
• W4283731304 hasRelatedWork W3199816176 @default.
• W4283731304 hasRelatedWork W4283731304 @default.
• W4283731304 hasVolume "37" @default.
• W4283731304 isParatext "false" @default.
• W4283731304 isRetracted "false" @default.
• W4283731304 workType "article" @default.