http://purl.uniprot.org/citations/25692550 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25692550 | http://www.w3.org/2000/01/rdf-schema#comment | "We aimed to study the role of the nucleotide receptor P2Y2R in the development of experimental autoimmune uveitis (EAU). EAU was induced in P2Y2+/+ and P2Y2-/-mice by immunization with IRBP peptide or by adoptive transfer of in vitro restimulated semi-purified IRBP-specific enriched T lymphocytes from spleens and lymph nodes isolated from native C57Bl/6 or P2Y2+/+ and P2Y2-/-immunized mice. Clinical and histological scores were used to grade disease severity. Splenocytes and lymph node cell phenotypes were analyzed using flow cytometry. Semi-purified lymphocytes and MACS-purified CD4+ T lymphocytes from P2Y2+/+ and P2Y2-/-immunized mice were tested for proliferation and cytokine secretion. Our data show that clinical and histological scores were significantly decreased in IRBP-immunized P2Y2-/- mice as in P2Y2-/-mice adoptively transfered with enriched T lymphocytes from C57Bl/6 IRBP-immunized mice. In parallel, naïve C57Bl/6 mice adoptively transferred with T lymphocytes from P2Y2-/-IRBP-immunized mice also showed significantly less disease. No differences in term of spleen and lymph node cell recruitment or phenotype appeared between P2Y2-/- and P2Y2+/+ immunized mice. However, once restimulated in vitro with IRBP, P2Y2-/-T cells proliferate less and secrete less cytokines than the P2Y2+/+ one. We further found that antigen-presenting cells of P2Y2-/-immunized mice were responsible for this proliferation defect. Together our data show that P2Y2-/-mice are less susceptible to mount an autoimmune response against IRBP. Those results are in accordance with the danger model, which makes a link between autoreactive lymphocyte activation, cell migration and the release of danger signals such as extracellular nucleotides."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0116518"xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Communi D."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Robaye B."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Bruyns C."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Boeynaems J.M."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Caspers L."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Willermain F."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Dewispelaere R."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Makhoul M."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/author | "Relvas L.J."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/pages | "e0116518"xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/title | "P2Y2R deficiency attenuates experimental autoimmune uveitis development."xsd:string |
http://purl.uniprot.org/citations/25692550 | http://purl.uniprot.org/core/volume | "10"xsd:string |
http://purl.uniprot.org/citations/25692550 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25692550 |
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http://purl.uniprot.org/uniprot/P35383 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25692550 |