Journal of Leukocyte Biology
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A more recent version of this article appeared on August 1, 2007

Published online before print April 30, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0107021

Received for publication January 10, 2007.
Revised April 7, 2007.
Accepted for publication April 9, 2007.

Article

Regulation of TLR4 signaling and the host interface with pathogens and danger: the role of RP105

Senad Divanovic *, Aurelien Trompette *, Lisa K. Petiniot *, Jessica L. Allen *, Leah M. Flick *, Yasmine Belkaid {dagger}, Rajat Madan *, Jennifer J. Haky *, and Christopher L. Karp *@

*Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; and {dagger}Mucosal Immunology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA

@ To whom correspondence should be addressed. E-mail: chris.karp{at}chmcc.org.


  Abstract

As all immune responses have potential for damaging the host, tight regulation of such responses--in amplitude, space, time, and character--is essential for maintaining health and homeostasis. It was thus inevitable that the initial wave of papers about the role of TLRs, nucleotide-binding oligomerization domain-like receptors, and retinoic acid-inducible gene-I-like receptors in activating innate and adaptive immune responses would be followed by a second wave of reports focusing on the mechanisms responsible for restraining and modulating signaling by these receptors. This overview outlines current knowledge and controversies about the immunobiology of the radioprotective 105 kD/myeloid differentiation protein 1 complex, a modulator of the most robustly signaling TLR, TLR4.

Key Words: MD-1 • endogenous ligand • counter-regulation






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Copyright © 2007 by the Society for Leukocyte Biology.