| First Author | Shaw PJ | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 9 | Pages | 4610-4 |
| PubMed ID | 20368281 | Mgi Jnum | J:160438 |
| Mgi Id | MGI:4454467 | Doi | 10.4049/jimmunol.1000217 |
| Citation | Shaw PJ, et al. (2010) Cutting Edge: critical role for PYCARD/ASC in the development of experimental autoimmune encephalomyelitis. J Immunol 184(9):4610-4 |
| abstractText | 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. |
