期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 9, 页码 4610-4614出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000217
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资金
- National Institutes of Health [AR056296]
- American Lebanese and Syrian Associated Charities
Multiple sclerosis is an autoimmune disease in which self-reactive T cells attack oligodendrocytes that myelinate axons in the CNS. Experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, is dependent on caspase-1; however, the role of Nod-like receptors upstream of caspase-1 is unknown. Danger- and pathogen-associated molecular patterns activate Nod-like receptor 3, which activates caspase-1 through the adaptor protein, apoptosis-associated speck-like protein containing CARD (ASC). We report that the progression of EAE is dependent on ASC and caspase-1 but not Nod-like receptor 3. ASC(-/-) mice were even more protected from the progression of EAE than were caspase-1(-/-) mice, suggesting that an inflammasome-independent function of ASC contributes to the progression of EAE. We found that CD4(+) T cells deficient in ASC exhibited impaired survival; accordingly, ASC(-/-) mice had fewer myelin oligodendrocyte glycoprotein specific T cells in the draining lymph nodes and CNS. The Journal of Immunology, 2010, 184: 4610-4614.
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