http://purl.uniprot.org/citations/35378447 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/35378447 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundInterleukin-33 (IL-33) is a member of the interleukin-1 family, which is reported to be important across a range of diseases. However, the mechanisms underlying IL-33/ST2 axis in infectious diseases have not yet been fully addressed.MethodsWe established both lipopolysaccharide (LPS)-induced injuryin T cells and Listeria monocytogenes (Lm) infection model to determine the effect of IL-33 on infectious immunity.ResultsThe T cell proliferation was inhibited by LPS while IL-33 could reverse the outcome. Further, apoptosis was significantly promoted after serum stimulation (ST)2 knockdown, suggesting IL-33, acting through its receptor ST2, may attenuate the inhibitory effect of LPS on T cells through the apoptotic signaling pathway. In this study, we also identified an IL-33-mediated mechanism of T cell differentiation in pregnant mice infected with Lm. Here, we observed the elevated expression of IL-33 in pregnant mice infected with Lm. Furthermore, we revealed that blocking IL-33 markedly decreased the abortion rate and placental bacterial load, but weakened placental inflammatory repair, by inhibiting Th2 cell-mediated immune responses and relatively intensifying Th1-dominent immunoreaction.ConclusionsThese findings reveal a previously unidentified mechanism underlying IL-33/ST2 axis. IL-33 signaling and targeting T cell-mediated immunity may present a new therapeutic strategy for the treatment of infectious diseases."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.intimp.2022.108742"xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Li C."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Li Y."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Zhang T."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Yu X."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Yin C."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Peng Y."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/author | "Luan Y."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/name | "Int Immunopharmacol"xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/pages | "108742"xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/title | "The potential role and regulatory mechanism of IL-33/ST2 axis on T lymphocytes during lipopolysaccharide stimulation or perinatal Listeria infection."xsd:string |
http://purl.uniprot.org/citations/35378447 | http://purl.uniprot.org/core/volume | "108"xsd:string |
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