TY - JOUR
T1 - Regulatory roles for MD-2 and TLR4 in ligand-induced receptor clustering
AU - Kobayashi, Makiko
AU - Saitoh, Shin Ichiroh
AU - Tanimura, Natsuko
AU - Takahashi, Koichiro
AU - Kawasaki, Kiyoshi
AU - Nishijima, Masahiro
AU - Fujimoto, Yukari
AU - Fukase, Koichi
AU - Akashi-Takamura, Sachiko
AU - Miyake, Kensuke
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2006/5/15
Y1 - 2006/5/15
N2 - LPS, a principal membrane component in Gram-negative bacteria, is recognized by a receptor complex consisting of TLR4 and MD-2. MD-2 is an extracellular molecule that is associated with the extracellular domain of TLR4 and has a critical role in LPS recognition. MD-2 directly interacts with LPS, and the region from Phe119 to Lys132 (Arg132 in mice) has been shown to be important for interaction between LPS and TLR4/MD-2. With mouse MD-2 mutants, we show in this study that Gly59 was found to be a novel critical amino acid for LPS binding outside the region 119-132. LPS signaling is thought to be triggered by ligand-induced TLR4 clustering, which is also regulated by MD-2. Little is known, however, about a region or an amino acid in the MD-2 molecule that regulates ligand-induced receptor clustering. MD-2 mutants substituting alanine for Phe126 or Gly 129 impaired LPS-induced TLR4 clustering, but not LPS binding to TLR4/MD-2, demonstrating that ligand-induced receptor clustering is differentially regulated by MD-2 from ligand binding. We further show that dissociation of ligand-induced receptor clustering and of ligand-receptor interaction occurs in a manner dependent on TLR4 signaling and requires endosomal acidification. These results support a principal role for MD-2 in LPS recognition.
AB - LPS, a principal membrane component in Gram-negative bacteria, is recognized by a receptor complex consisting of TLR4 and MD-2. MD-2 is an extracellular molecule that is associated with the extracellular domain of TLR4 and has a critical role in LPS recognition. MD-2 directly interacts with LPS, and the region from Phe119 to Lys132 (Arg132 in mice) has been shown to be important for interaction between LPS and TLR4/MD-2. With mouse MD-2 mutants, we show in this study that Gly59 was found to be a novel critical amino acid for LPS binding outside the region 119-132. LPS signaling is thought to be triggered by ligand-induced TLR4 clustering, which is also regulated by MD-2. Little is known, however, about a region or an amino acid in the MD-2 molecule that regulates ligand-induced receptor clustering. MD-2 mutants substituting alanine for Phe126 or Gly 129 impaired LPS-induced TLR4 clustering, but not LPS binding to TLR4/MD-2, demonstrating that ligand-induced receptor clustering is differentially regulated by MD-2 from ligand binding. We further show that dissociation of ligand-induced receptor clustering and of ligand-receptor interaction occurs in a manner dependent on TLR4 signaling and requires endosomal acidification. These results support a principal role for MD-2 in LPS recognition.
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U2 - 10.4049/jimmunol.176.10.6211
DO - 10.4049/jimmunol.176.10.6211
M3 - Article
C2 - 16670331
AN - SCOPUS:33646494167
SN - 0022-1767
VL - 176
SP - 6211
EP - 6218
JO - Journal of Immunology
JF - Journal of Immunology
IS - 10
ER -