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 Blood, 30 April 2009, Vol. 113, No. 18, pp. 4224-4231.
Prepublished online as a Blood First Edition Paper on February 6, 2009; DOI 10.1182/blood-2008-08-174698.

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Submitted August 19, 2008
Accepted January 16, 2009

A TLR2 ligand suppresses inflammation by modulation of chemokine receptors and redirection of leukocyte migration

Clive S. McKimmie, Mark Moore, Alasdair R. Fraser, Thomas Jamieson, Damo Xu, Claire Burt, Nick I. Pitman, Robert J. Nibbs, Iain B. McInnes, Foo Y. Liew, and Gerard J. Graham*

Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow Biomedical Research Centre, Glasgow, United Kingdom
Beatson Institute for Cancer Research, Glasgow, United Kingdom

* Corresponding author; email: g.graham{at}clinmed.gla.ac.uk.

Toll-like receptors orchestrate rapid local protective innate-immune responses to invading pathogens and optimise leukocyte priming of subsequent adaptive responses. Paradoxically systemic excess of the TLR2 ligand, Bacterial Lipoprotein, suppresses peripheral inflammatory responses. We here 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 towards 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.


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