Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Originally published online as doi:10.1189/jlb.0304127 on June 3, 2004

Published online before print June 3, 2004
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(Journal of Leukocyte Biology. 2004;76:514-519.)
© 2004 by Society for Leukocyte Biology

Endogenous ligands of Toll-like receptors

Min-Fu Tsan*,{dagger},1 and Baochong Gao*,{ddagger}

* Research Service, VA Medical Center, Washington, DC;
{dagger} Department of Medicine, Georgetown University, Washington, DC; and
{ddagger} Department of Medicine, George Washington University, Washington, DC

1 Correspondence: Mid-Atlantic Regional Office (10R), Office of Research Oversight, Department of Veterans Affairs, 50 Irving Street, NW, Washington, DC 20422. E-mail: min-fu.tsan2{at}med.va.gov

Extensive work has suggested that a number of endogenous molecules such as heat shock proteins (hsp) may be potent activators of the innate immune system capable of inducing proinflammatory cytokine production by the monocyte-macrophage system and the activation and maturation of dendritic cells. The cytokine-like effects of these endogenous molecules are mediated via the Toll-like receptor (TLR) signal-transduction pathways in a manner similar to lipopolysaccharide (LPS; via TLR4) and bacterial lipoproteins (via TLR2). However, recent evidence suggests that the reported cytokine effects of hsp may be a result of the contaminating LPS and LPS-associated molecules. The reasons for previous failure to recognize the contaminant(s) being responsible for the putative TLR ligands of hsp include failure to use highly purified hsp free of LPS contamination; failure to recognize the heat sensitivity of LPS; and failure to consider contaminant(s) other than LPS. Whether other reported putative endogenous ligands of TLR2 and TLR4 are a result of contamination of pathogen-associated molecular patterns is not clear. It is essential that efforts should be directed to conclusively determine whether the reported putative endogenous ligands of TLRs are a result of the endogenous molecules or of contaminant(s), before exploring further the implication and therapeutic potential of these putative TLR ligands.

Key Words: endotoxin • danger signal • pathogen-associated molecular patterns




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