期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 1, 页码 17-21出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.1.17
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- NINDS NIH HHS [3R01 NS 32151] Funding Source: Medline
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) piptide 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 De(+/+) littermates. In adoptive transfer studies, MOG-primed De(+/-) 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-gamma 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.
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