Article

Cutting edge: critical role for PYCARD/ASC in the development of experimental autoimmune encephalomyelitis.

Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38104, USA.
The Journal of Immunology (impact factor: 5.79). 04/2010; 184(9):4610-4. DOI:10.4049/jimmunol.1000217 pp.4610-4
Source: PubMed

ABSTRACT 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.

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    Article: The role of inflammasome-derived IL-1 in driving IL-17 responses.
    Kingston H G Mills, Lara S Dungan, Sarah A Jones, James Harris
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    Journal of leukocyte biology 12/2012; · 4.99 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

activates caspase-1
 
adaptor protein
 
apoptosis-associated speck-like protein
 
ASC contributes
 
ASC exhibited
 
autoimmune disease
 
dependent
 
draining lymph nodes
 
Experimental autoimmune encephalomyelitis
 
inflammasome-independent function
 
multiple sclerosis
 
myelin oligodendrocyte glycoprotein-specific T cells
 
myelinate axons
 
Nod-like receptor 3. ASC(-/-)
 
Nod-like receptors upstream
 
pathogen-associated molecular patterns activate Nod-like receptor 3
 
self-reactive T cells attack oligodendrocytes