| Sign In to gain access to subscriptions and/or personal tools. |
The role of Toll-like receptors and MyD88 in innate immune responsesDepartment of Host Defense, Research Institute for Microbial Diseases, Osaka University; CREST of Japan Science and Technology Corporation, Osaka, Japan, sakira{at}biken.osaka-u.ac.jp
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University; CREST of Japan Science and Technology Corporation, Osaka, Japan
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University; CREST of Japan Science and Technology Corporation, Osaka, Japan
Toll-like receptors (TLRs) are phylogenetically conserved receptors that recognize pathogen associated molecular patterns (PAMPS). We previously generated mice lacking TLR2 and TLR4 and showed the differential role of TLR2 and TLR4 in microbial recognition. TLR4 functions as the transmembrane component of the lipopolysaccharide (LPS) receptor, while TLR2 recognizes peptidoglycan from Gram-positive bacteria and lipoprotein. We also generated mice lacking MyD88, an adaptor involved in IL-1R/TLR signalings. The responses to a variety of bacterial components were completely abrogated in MyD88-deficient cells. However, unlike the signaling mediated by other bacterial components such as lipoprotein and bacterial DNA, activation of NF-
Journal of Endotoxin Research, Vol. 6, No. 5,
383-387 (2000) |
|||
 |
|
|
 |
|
Sign In to gain access to subscriptions and/or personal tools.
B and MAP kinases was induced in response to LPS even in the absence of MyD88, which indicates the existence of a MyD88-independent pathway. We have recently found that the MyD88-independent pathway is involved in LPS-induced maturation of dendritic cells (DCs).