IL-1 receptor-associated kinase 1 regulates susceptibility to organ-specific autoimmunity.

Infections often precede the development of autoimmunity. Correlation between infection with a specific pathogen and a particular autoimmune disease ranges from moderately strong to quite weak. This lack of correspondence suggests that autoimmunity may result from microbial activation of a generic, as opposed to pathogen-specific host-defense response.

CpG DNA induced IL-12 p40 gene activation is independent of STAT1 activation or production of interferon consensus sequence binding protein.

The host immune system responds to CpG motifs in bacterial DNA by rapidly producing proinflammatory cytokines. The host response to CpG DNA resembles, in many ways, the response to bacterial lipopolysaccharide (LPS). While both agents can induce a powerful inflammatory response, CpG DNA promotes Th1 and suppresses Th2 immunity.