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- W2140179741 abstract "Experimental autoimmune encephalomyelitis (EAE), a Th1-mediated inflammatory disease of the central nervous system (CNS), is a model of human multiple sclerosis. Cytosolic phospholipase A2α (cPLA2α), which initiates production of prostaglandins, leukotrienes, and platelet-activating factor, is present in EAE lesions. Using myelin oligodendrocyte glycoprotein (MOG) immunization, as well as an adoptive transfer model, we showed that cPLA2α−/− mice are resistant to EAE. Histologic examination of the CNS from MOG-immunized mice revealed extensive inflammatory lesions in the cPLA2α+/− mice, whereas the lesions in cPLA2α−/− mice were reduced greatly or completely absent. MOG-specific T cells generated from WT mice induced less severe EAE in cPLA2α−/− mice compared with cPLA2α+/− mice, which indicates that cPLA2α plays a role in the effector phase of EAE. Additionally, MOG-specific T cells from cPLA2α−/− mice, transferred into WT mice, induced EAE with delayed onset and lower severity compared with EAE that was induced by control cells; this indicates that cPLA2α also plays a role in the induction phase of EAE. MOG-specific T cells from cPLA2α−/− mice were deficient in production of Th1-type cytokines. Consistent with this deficiency, in vivo administration of IL-12 rendered cPLA2α−/− mice susceptible to EAE. Our data indicate that cPLA2α plays an important role in EAE development and facilitates differentiation of T cells toward the Th1 phenotype." @default.
- W2140179741 created "2016-06-24" @default.
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- W2140179741 date "2005-09-19" @default.
- W2140179741 modified "2023-10-16" @default.
- W2140179741 title "Cytosolic phospholipase A2α–deficient mice are resistant to experimental autoimmune encephalomyelitis" @default.
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- W2140179741 doi "https://doi.org/10.1084/jem.20050665" @default.
- W2140179741 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2212947" @default.
- W2140179741 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16172261" @default.
- W2140179741 hasPublicationYear "2005" @default.
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