Abstract:
:Toll-like receptors orchestrate rapid local protective innate-immune responses to invading pathogens and optimize leukocyte priming of subsequent adaptive responses. Paradoxically, systemic excess of the TLR2 ligand, bacterial lipoprotein (BLP), suppresses peripheral inflammatory responses. Here, we demonstrate that this phenomenon is regulated via the TLR2-dependent, cell-autonomous down-regulation of inflammatory chemokine receptor expression on a variety of leukocyte subsets. Remarkably, BLP mediated no effect on constitutive chemokine receptor expression. By tracking adoptively transferred wild-type and TLR2(-/-) leukocytes in vivo, we observed that BLP mediated chemokine receptor switching directed leukocytes away from inflamed sites toward secondary lymphoid organs. These data highlight a novel role for TLR ligands, such as BLP, in regulating leukocyte retention and migration away from innate immune lesions via discrete constitutive and inflammatory chemokine receptor regulation.
journal_name
Bloodjournal_title
Bloodauthors
McKimmie CS,Moore M,Fraser AR,Jamieson T,Xu D,Burt C,Pitman NI,Nibbs RJ,McInnes IB,Liew FY,Graham GJdoi
10.1182/blood-2008-08-174698subject
Has Abstractpub_date
2009-04-30 00:00:00pages
4224-31issue
18eissn
0006-4971issn
1528-0020pii
blood-2008-08-174698journal_volume
113pub_type
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