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Published online before print April 30, 2007

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(Journal of Leukocyte Biology. 2007;82:265-271.)
© 2007 by Society for Leukocyte Biology

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, Rajat Madan^*, Jennifer J. Haky^* and Christopher L. Karp^*,1

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

¹ Correspondence: Division of Molecular Immunology, Cincinnati Children’s Hospital Research Foundation, 3333 Burnet Avenue, Cincinnati, OH 45229, USA. 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 on the role of Toll-like receptors (TLRs), NOD-like receptors (NLRs) and RIG-I-like receptors (RLRs) 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 RP105/MD-1 complex, a modulator of the most robustly signaling TLR, TLR4.

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

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