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Toll-like receptors (TLRs) have been revealed to recognize specific patterns of microbial components. Recognition of microbial components by TLRs initiates signal transduction pathways, triggering expression of genes, which products control innate immune responses and further instruct development of antigen-specific acquired immunity. TIR domain-containing adaptors, such as MyD88, TIRAP, TRIF, and TRAM, play pivotal roles in TLR signaling pathways. Differential utilization of these TIR domain-containing adaptors provides specificity of individual TLR-mediated signaling pathways. TLR-mediated activation of innate immunity, when in excess, leads to immune disorders such as inflammatory bowel diseases. Therefore, several mechanisms that negatively control TLR signaling pathways and thereby prevent overactivation of innate immunity have been elucidated. Nuclear IkappaB proteins, such as Bcl-3 and IkappaBNS, have been revealed to be responsible for this process, by differentially inhibiting TLR-dependent cytokine production.

自己免疫性疾患の病態形成に関わる細胞・分子と臨床応用 Ｔｏｌｌ‐ｌｉｋｅ ｒｅｃｅｐｔｏｒと炎症性腸疾患

自己免疫性疾患の病態形成に関わる細胞・分子と臨床応用Ｔｏｌｌ‐ｌｉｋｅｒｅｃｅｐｔｏｒと炎症性腸疾患