open access

https://hdl.handle.net/2115/43949

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

英語

CD36

2010-06-01

Blackwell Scientific Publications

Immunology : an official journal of the British Society for Immunology

130(2)

262-272

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.

学術雑誌論文

Accepted Manuscript

0019-2805

1365-2567

AA00670257