Evolution and integration of innate immune recognition systems: the Toll-like receptors.
Toll-like receptors (TLRs) recognize specific components of micro-organisms and trigger the activation of innate immunity. TLR-mediated signaling pathways are now rapidly being elucidated. TLR signaling originates from the cytoplasmic Toll/IL-1 receptor (TIR) domain, which is conserved among all TLRs. Furthermore, TIR domain-containing adaptors, such as MyD88, TRIF, TIRAP and TRAM, play essential roles in TLR signaling. MyD88 is essential for inflammatory cytokine production via all TLRs, whereas TRIF is involved in TLR3- and TLR4-mediated MyD88-independent induction of IFN-beta. Thus, innate immunity represents a skillful system that senses microbial invasion and initiates appropriate immune responses.
Takeda
Kiyoshi
K
Department of Molecular Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan. ktakeda@bioreg.kyushu-u.ac.jp
D033942:Adaptor Proteins, Vesicular Transport / Q000276:immunology / Q000378:metabolism; D000818:Animals; D005075:Biological Evolution; D006801:Humans; D007113:Immunity, Innate; D008562:Membrane Glycoproteins / Q000276:immunology* / Q000378:metabolism*; D008954:Models, Biological; D011956:Receptors, Cell Surface / Q000276:immunology* / Q000378:metabolism*; D051196:Toll-Like Receptor 3; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors
D033942:Adaptor Proteins, Vesicular Transport; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C470409:TICAM1 protein, human; C495344:TLR3 protein, human; C495345:TLR4 protein, human; D051196:Toll-Like Receptor 3; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors