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The TLR2 ligand FSL-1 is internalized via clathrin-dependent endocytic pathway triggered by CD14 and CD36 but not by TLR2

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Title: The TLR2 ligand FSL-1 is internalized via clathrin-dependent endocytic pathway triggered by CD14 and CD36 but not by TLR2
Authors: Haque, Shamsul Browse this author
Hasebe, Akira Browse this author →KAKEN DB
Iyori, Mitsuhiro Browse this author
Ohtani, Makoto Browse this author
Kiura, Kazuto Browse this author
Zhang, Diya Browse this author
Totsuka, Yasunori Browse this author
Shibata, Ken-ichiro Browse this author
Keywords: TLR2
clathrin-dependent endocytosis
Issue Date: 1-Jun-2010
Publisher: Blackwell Scientific Publications
Journal Title: Immunology : an official journal of the British Society for Immunology
Volume: 130(2)
Start Page: 262
End Page: 272
Publisher DOI: 10.1111/j.1365-2567.2009.03232.x
PMID: 20113368
Abstract: Little is known about how Toll-like receptor (TLR) ligands are processed after recognition by TLRs. This study was therefore designed to investigate how the TLR2 ligand FSL-1 is processed in macrophages after recognition by TLR2. FSL-1 was internalized into murine macrophage cell line, RAW264.7. Both chlorpromazine and methyl-β-cyclodextrin, which inhibit clathrin-dependent endocytosis, reduced FSL-1 uptake by RAW264.7 cells in a dose-dependent manner, but nystatin which inhibits caveolae- and lipid raft-dependent endocytosis, did not. FSL-1 was colocalized with clathrin but not with TLR2 in the cytosol of RAW264.7 cells. These results suggest that internalization of FSL-1 is clathrin dependent. In addition, FSL-1 was internalized by peritoneal macrophages from TLR2-deficient mice. FSL-1 was internalized by human embryonic kidney 293 cells transfected with CD14 or CD36 but not by the non-transfected cells. Also, knockdown of CD14 or CD36 in the transfectants reduced FSL-1 uptake In this study, we suggest that (i) FSL-1 is internalized into macrophages via a clathrin-dependent endocytic pathway, (ii) the FSL-1 uptake by macrophages occurs irrespective of the presence of TLR2, and (iii) CD14 and CD36 are responsible for the 18 internalization of FSL-1.
Type: article (author version)
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 柴田 健一郎

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