Critical roles of c-Rel in autoimmune inflammation and helper T cell differentiation
AUTOR(ES)
Hilliard, Brendan A.
FONTE
American Society for Clinical Investigation
RESUMO
Different members of the Rel/NF-κB family may play different roles in immunity and inflammation. We report here that c-Rel–deficient mice are resistant to autoimmune encephalomyelitis and are defective in Th1, but not Th2 responses. The Th1 deficiency appears to be caused by selective blockade of IL-12 production by c-Rel–deficient antigen-presenting cells, as well as by a complete abrogation of IFN-γ expression in c-Rel–deficient T cells. Interestingly, c-Rel deficiency does not affect T-bet expression, suggesting that c-Rel may act downstream of T-bet during Th1 cell differentiation. Thus, unlike NF-κB1, which selectively regulates Th2 cell differentiation, c-Rel is essential for Th1 cell differentiation and Th1 cell–mediated autoimmune inflammation.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=151124Documentos Relacionados
- c-Rel delivers a one-two punch in Th1 cell differentiation
- Specific NEMO mutations impair CD40-mediated c-Rel activation and B cell terminal differentiation
- Transformation of avian fibroblasts overexpressing the c-rel proto-oncogene and a variant of c-rel lacking 40 C-terminal amino acids.
- In vivo evolution of c-rel oncogenic potential.
- Genetic characterization of human c-rel sequences.