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The Journal of Immunology, 2006, 177: 1272-1281.
Copyright © 2006 by The American Association of Immunologists

Hyaluronan Fragments Act as an Endogenous Danger Signal by Engaging TLR21

Kara A. Scheibner*, Michael A. Lutz{dagger}, Sada Boodoo*, Matthew J. Fenton2,{ddagger}, Jonathan D. Powell{dagger} and Maureen R. Horton3,*

* Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205; {dagger} Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231; and {ddagger} Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201

Upon tissue injury, high m.w. hyaluronan (HA), a ubiquitously distributed extracellular matrix component, is broken down into lower m.w. (LMW) fragments, which in turn activate an innate immune response. In doing so, LMW HA acts as an endogenous danger signal alerting the immune system of a breach in tissue integrity. In this report, we demonstrate that LMW HA activates the innate immune response via TLR-2 in a MyD88-, IL-1R-associated kinase-, TNFR-associated factor-6-, protein kinase C{zeta}-, and NF-{kappa}B-dependent pathway. Furthermore, we show that intact high m.w. HA can inhibit TLR-2 signaling. Finally, we demonstrate that LMW HA can act as an adjuvant promoting Ag-specific T cell responses in vivo in wild-type but not TLR-2null mice.




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