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- W2113804090 abstract "Abstract D6, a promiscuous nonsignaling chemokine binding molecule expressed on the lymphatic endothelium, internalizes and degrades CC chemokines, and D6−/− mice demonstrated increased cutaneous inflammation following topical phorbol ester or CFA injection. We report that D6−/− mice were unexpectedly resistant to the induction of experimental autoimmune encephalomyelitis due to impaired encephalitogenic responses. Following induction with myelin oligodendroglial glycoprotein (MOG) peptide 35–55 in CFA, D6−/− mice showed reduced spinal cord inflammation and demyelination with lower incidence and severity of experimental autoimmune encephalomyelitis attacks as compared with D6+/+ littermates. In adoptive transfer studies, MOG-primed D6+/− T cells equally mediated disease in D6+/+ or D6−/− mice, whereas cells from D6−/− mice transferred disease poorly to D6+/− recipients. Lymph node cells from MOG-primed D6−/− mice showed weak proliferative responses and made reduced IFN-γ but normal IL-5. CD11c+ dendritic cells accumulated abnormally in cutaneous immunization sites of D6−/− mice. Surprisingly, D6, a “silent” chemokine receptor, supports immune response generation." @default.
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- W2113804090 date "2006-07-01" @default.
- W2113804090 modified "2023-10-01" @default.
- W2113804090 title "Cutting Edge: The Silent Chemokine Receptor D6 Is Required for Generating T Cell Responses That Mediate Experimental Autoimmune Encephalomyelitis" @default.
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- W2113804090 doi "https://doi.org/10.4049/jimmunol.177.1.17" @default.
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