Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.1206752 on May 10, 2007

Published online before print May 10, 2007
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(Journal of Leukocyte Biology. 2007;82:282-285.)
© 2007 by Society for Leukocyte Biology

Pivotal Advance: Endogenous pathway to SIRS, sepsis, and related conditions

Amy H. Tang*,{dagger},{ddagger}, Gregory J. Brunn*,§, Marilia Cascalho*,{dagger},||,¶ and Jeffrey L. Platt*,{dagger},||,¶,1

* Transplantation Biology Program and the Departments of
{dagger} Surgery,
{ddagger} Biochemistry and Molecular Biology,
§ Pharmacology,
|| Immunology, and
Pediatrics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA

1 Correspondence: Transplantation Biology, Mayo Clinic, 200 First Street, S.W., Medical Sciences 2-66, Rochester, MN 55905, USA. E-mail: platt.jeffrey{at}mayo.edu

ABSTRACT

TLRs are usually thought to recognize substances produced by microorganisms and thus, to initiate host defenses. This concept, however, fails to explain some functions of this family of receptors. Recognition of endogenous substances may explain the broader functions of TLRs in physiology and disease. Activation of TLRs by endogenous substances necessitates vigorous control of the function of the receptors. This communication will summarize a line of research, which points to an endogenous agonist for TLR4 and a putative mechanism for controlling the function of that receptor.

Key Words: Toll-like receptors • systemic inflammatory response syndrome • heparan sulfate


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