| http://purl.uniprot.org/citations/17525267 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17525267 | http://www.w3.org/2000/01/rdf-schema#comment | "p150/95 (CD11c/CD18, CR4) is a member of the beta(2)-integrin family of adhesion molecules and is considered an important phagocytic receptor. The role of p150/95 in the development of central nervous system demyelinating diseases, including multiple sclerosis, remains unexplored. To determine p150/95-mediated mechanisms in experimental autoimmune encephalomyelitis (EAE), we performed EAE using CD11c-deficient (CD11c(-/-)) mice. EAE in CD11c(-/-) mice was significantly attenuated and characterized by markedly reduced spinal cord T-cell infiltration and interferon-gamma production by these cells. Adoptive transfer of antigen-restimulated T cells from wild-type to CD11c(-/-) mice produced significantly attenuated EAE, whereas transfer of CD11c(-/-) antigen-restimulated T cells to control mice induced a very mild, monophasic EAE. T cells from MOG(35-55) peptide-primed CD11c(-/-) mice displayed an unusual cytokine phenotype with elevated levels of interleukin (IL)-2, IL-4, and IL-12 but reduced levels of interferon-gamma, tumor necrosis factor-alpha, IL-10, IL-17, and transforming growth factor-beta compared with control mice. Overall, CD11c(-/-) T cells from primed mice proliferated comparably to that of control T cells on MOG(35-55) restimulation. Our results indicate that expression of p150/95 is critical on both T cells as well as other leukocytes for the development of demyelinating disease and may represent a novel therapeutic target for multiple sclerosis."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.org/dc/terms/identifier | "doi:10.2353/ajpath.2007.061016"xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/author | "Hu X."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/author | "Barnum S.R."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/author | "Schoeb T.R."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/author | "Adams J.E."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/author | "Bullard D.C."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/name | "Am J Pathol"xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/pages | "2001-2008"xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/title | "p150/95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis."xsd:string |
| http://purl.uniprot.org/citations/17525267 | http://purl.uniprot.org/core/volume | "170"xsd:string |
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