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Signaling via the RIP2 adaptor protein in central nervous system-infiltrating dendritic cells promotes inflammation and autoimmunity.
Shaw, Patrick J; Barr, Maggie J; Lukens, John R; McGargill, Maureen A; Chi, Hongbo; Mak, Tak W; Kanneganti, Thirumala-Devi.
Afiliação
  • Shaw PJ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38104, USA.
Immunity ; 34(1): 75-84, 2011 Jan 28.
Article em En | MEDLINE | ID: mdl-21236705
Peripheral peptidolgycan (PGN) is present within antigen-presenting cells in the central nervous system (CNS) of multiple sclerosis (MS) patients, possibly playing a role in neuroinflammation. Accordingly, PGN is linked with disease progression in the animal model of MS, experimental autoimmune encephalomyelitis (EAE), but the role of specific PGN-sensing proteins is unknown. Here we report that the progression of EAE was dependent on the intracellular PGN sensors NOD1 and NOD2 and their common downstream adaptor molecule, receptor interacting protein 2 (RIP2; also known as RIPK2 and RICK). We found that RIP2, but not toll-like receptor 2 (TLR2), played a critical role in the activation of CNS-infiltrating dendritic cells. Our results suggest that PGN in the CNS is involved in the pathogenesis of EAE through the activation of infiltrating dendritic cells via NOD1-, NOD2-, and RIP2-mediated pathways.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Células Dendríticas / Sistema Nervoso Central / Encefalomielite Autoimune Experimental / Proteína Serina-Treonina Quinases de Interação com Receptores / Esclerose Múltipla Limite: Animals / Humans Idioma: En Ano de publicação: 2011 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Células Dendríticas / Sistema Nervoso Central / Encefalomielite Autoimune Experimental / Proteína Serina-Treonina Quinases de Interação com Receptores / Esclerose Múltipla Limite: Animals / Humans Idioma: En Ano de publicação: 2011 Tipo de documento: Article