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http://purl.uniprot.org/citations/24107315http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24107315http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24107315http://www.w3.org/2000/01/rdf-schema#comment"Glucocorticoid-induced TNF receptor family-related protein (GITR) regulates the function of both T cells and antigen-presenting cells (APCs), while the function of GITR ligand (GITR-L) is largely unknown. Here we evaluate the role of GITR-L, whose expression is restricted to APCs, in the development of enterocolitis. On injecting naive CD4(+) T cells, GITR-L(-/-)Rag(-/-) mice develop a markedly milder colitis than Rag(-/-) mice, which correlates with a 50% reduction of Ly6C(+)CD11b(+)MHCII(+) macrophages in the lamina propria and mesenteric lymph nodes. The same result was observed in αCD40-induced acute colitis and during peritonitis, suggesting an altered monocyte migration. In line with these observations, the number of nondifferentiated monocytes was approximately 3-fold higher in the spleen of GITR-L(-/-)Rag(-/-) mice than in Rag(-/-) mice after αCD40 induction. Consistent with the dynamic change in the formation of an active angiotensin II type 1 receptor (AT1) dimer in GITR-L(-/-) splenic monocytes during intestinal inflammation, the migratory capability of splenic monocytes from GITR-L-deficient mice was impaired in an in vitro transwell migration assay. Conversely, αGITR-L reduces the number of splenic Ly6C(hi) monocytes, concomitantly with an increase in AT1 dimers. We conclude that GITR-L regulates the number of proinflammatory macrophages in sites of inflammation by controlling the egress of monocytes from the splenic reservoir."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.org/dc/terms/identifier"doi:10.1096/fj.13-236505"xsd:string
http://purl.uniprot.org/citations/24107315http://purl.org/dc/terms/identifier"doi:10.1096/fj.13-236505"xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Liao G."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Liao G."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Engel P."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Engel P."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Bhan A.K."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Bhan A.K."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Terhorst C."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Terhorst C."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Mizoguchi E."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Mizoguchi E."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"de Waal Malefyt R."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"de Waal Malefyt R."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Herzog R.W."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Herzog R.W."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"O'Keeffe M.S."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"O'Keeffe M.S."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Magelky E."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"Magelky E."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"van Driel B."xsd:string
http://purl.uniprot.org/citations/24107315http://purl.uniprot.org/core/author"van Driel B."xsd:string