FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2557573383> ?p ?o ?g. }

• W2557573383 endingPage "e2489" @default.
• W2557573383 startingPage "e2489" @default.
• W2557573383 abstract "Foxp3+ regulatory T (Treg) cells contribute to the local dysfunctional immune environment in endometriosis, an estrogen-dependent gynecological disease, which affects the function of ectopic endometrial tissue clearance by the immune system. The reason for the high percentage of peritoneal Treg in endometriosis patients is unknown. Here, we show that the proportion of peritoneal Treg cells increases as endometriosis progresses. To determine the probable mechanism, we established a naive T cell-macrophage-endometrial stromal cell (ESC) co-culture system to mimic the peritoneal cavity microenvironment. After adding 1-methyl-tryptophan (1-MT), a specific inhibitor of indoleamine 2,3-dioxygenase-1 (IDO1), to the co-culture system, we found that the differentiation of Treg cells, mainly IL-10+ Treg cells, decreased. Therefore, 1-MT-pretreated ESCs-educated Treg cells performed impaired suppressive function. Moreover, estrogen promoted the differentiation of Treg cells by elevating IDO1 expression in the ectopic lesion. Subsequently, we examined mannose receptor C, type 2 (MRC2), which is an up-stream molecule of IL-10, by bioinformatics analysis and real-time PCR validation. MRC2 expression in ectopic ESCs was notably lower than that in normal ESCs, which further negatively regulated the expression of IDO1 and Ki-67 in ESCs. Furthermore, MRC2 is required for Treg differentiation in the ectopic lesion, especially that for CD4high Treg. Therefore, MRC2-silenced ESCs-educated Treg manifested a stronger suppressive function in vitro. Consistently, the percentage of Treg increased when MRC2-shRNA was administered in the peritoneal cavity of endometriosis-disease mice model. Besides, 1-MT improved the condition of endometriosis, in terms of reducing the number and weight of total ectopic lesions in vivo. These results indicate that the estrogen-IDO1-MRC2 axis participates in the differentiation and function of Treg and is involved in the development of endometriosis. Thus, blockage of IDO1 in the ectopic lesion, which does not influence physiological functions of estrogen, may be considered a potential therapy for endometriosis." @default.
• W2557573383 created "2016-12-08" @default.
• W2557573383 creator A5002854902 @default.
• W2557573383 creator A5020532120 @default.
• W2557573383 creator A5031433768 @default.
• W2557573383 creator A5058510323 @default.
• W2557573383 creator A5077799326 @default.
• W2557573383 creator A5081126913 @default.
• W2557573383 creator A5087491415 @default.
• W2557573383 date "2016-12-01" @default.
• W2557573383 modified "2023-10-16" @default.
• W2557573383 title "1-Methyl-tryptophan attenuates regulatory T cells differentiation due to the inhibition of estrogen-IDO1-MRC2 axis in endometriosis" @default.
• W2557573383 cites W1505072916 @default.
• W2557573383 cites W1519185389 @default.
• W2557573383 cites W1520774369 @default.
• W2557573383 cites W156853574 @default.
• W2557573383 cites W1833987578 @default.
• W2557573383 cites W1897969243 @default.
• W2557573383 cites W1967404929 @default.
• W2557573383 cites W1972447650 @default.
• W2557573383 cites W1976085030 @default.
• W2557573383 cites W1989672313 @default.
• W2557573383 cites W1992662011 @default.
• W2557573383 cites W1996581577 @default.
• W2557573383 cites W2004755026 @default.
• W2557573383 cites W2009165570 @default.
• W2557573383 cites W2010378562 @default.
• W2557573383 cites W2011873300 @default.
• W2557573383 cites W2028366349 @default.
• W2557573383 cites W2042200211 @default.
• W2557573383 cites W2048798995 @default.
• W2557573383 cites W2052504614 @default.
• W2557573383 cites W2052758686 @default.
• W2557573383 cites W2079170656 @default.
• W2557573383 cites W2094533199 @default.
• W2557573383 cites W2110377638 @default.
• W2557573383 cites W2120423827 @default.
• W2557573383 cites W2121127545 @default.
• W2557573383 cites W2126266367 @default.
• W2557573383 cites W2134972751 @default.
• W2557573383 cites W2142359819 @default.
• W2557573383 cites W2148891929 @default.
• W2557573383 cites W2151338363 @default.
• W2557573383 cites W2151756326 @default.
• W2557573383 cites W2152508754 @default.
• W2557573383 cites W2153613808 @default.
• W2557573383 cites W2155602138 @default.
• W2557573383 cites W2157800695 @default.
• W2557573383 cites W2169410595 @default.
• W2557573383 cites W2234063371 @default.
• W2557573383 cites W4231488642 @default.
• W2557573383 doi "https://doi.org/10.1038/cddis.2016.375" @default.
• W2557573383 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5260991" @default.
• W2557573383 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27906184" @default.
• W2557573383 hasPublicationYear "2016" @default.
• W2557573383 type Work @default.
• W2557573383 sameAs 2557573383 @default.
• W2557573383 citedByCount "30" @default.
• W2557573383 countsByYear W25575733832017 @default.
• W2557573383 countsByYear W25575733832018 @default.
• W2557573383 countsByYear W25575733832019 @default.
• W2557573383 countsByYear W25575733832020 @default.
• W2557573383 countsByYear W25575733832021 @default.
• W2557573383 countsByYear W25575733832022 @default.
• W2557573383 countsByYear W25575733832023 @default.
• W2557573383 crossrefType "journal-article" @default.
• W2557573383 hasAuthorship W2557573383A5002854902 @default.
• W2557573383 hasAuthorship W2557573383A5020532120 @default.
• W2557573383 hasAuthorship W2557573383A5031433768 @default.
• W2557573383 hasAuthorship W2557573383A5058510323 @default.
• W2557573383 hasAuthorship W2557573383A5077799326 @default.
• W2557573383 hasAuthorship W2557573383A5081126913 @default.
• W2557573383 hasAuthorship W2557573383A5087491415 @default.
• W2557573383 hasBestOaLocation W25575733831 @default.
• W2557573383 hasConcept C105702510 @default.
• W2557573383 hasConcept C126322002 @default.
• W2557573383 hasConcept C134018914 @default.
• W2557573383 hasConcept C16930146 @default.
• W2557573383 hasConcept C203014093 @default.
• W2557573383 hasConcept C2777164284 @default.
• W2557573383 hasConcept C2778536324 @default.
• W2557573383 hasConcept C2779522080 @default.
• W2557573383 hasConcept C2779727006 @default.
• W2557573383 hasConcept C502942594 @default.
• W2557573383 hasConcept C71924100 @default.
• W2557573383 hasConcept C86803240 @default.
• W2557573383 hasConcept C8891405 @default.
• W2557573383 hasConceptScore W2557573383C105702510 @default.
• W2557573383 hasConceptScore W2557573383C126322002 @default.
• W2557573383 hasConceptScore W2557573383C134018914 @default.
• W2557573383 hasConceptScore W2557573383C16930146 @default.
• W2557573383 hasConceptScore W2557573383C203014093 @default.
• W2557573383 hasConceptScore W2557573383C2777164284 @default.
• W2557573383 hasConceptScore W2557573383C2778536324 @default.
• W2557573383 hasConceptScore W2557573383C2779522080 @default.
• W2557573383 hasConceptScore W2557573383C2779727006 @default.
• W2557573383 hasConceptScore W2557573383C502942594 @default.
• W2557573383 hasConceptScore W2557573383C71924100 @default.

• next