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The Journal of Immunology, 2003, 170: 3451-3454.
Copyright © 2003 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: A Toll-Like Receptor 2 Polymorphism That Is Associated with Lepromatous Leprosy Is Unable to Mediate Mycobacterial Signaling1

Pierre-Yves Bochud*, Thomas R. Hawn*,{dagger} and Alan Aderem2,*,{dagger}

* Institute for Systems Biology, Seattle, WA 98103; and {dagger} Division of Infectious Diseases, Department of Medicine, University of Washington, Seattle, WA 98195

Toll-like receptors (TLRs) are key mediators of the innate immune response to microbial pathogens. We investigated the role of TLRs in the recognition of Mycobacterium leprae and the significance of TLR2Arg677Trp, a recently discovered human polymorphism that is associated with lepromatous leprosy. In mice, TNF-{alpha} production in response to M. leprae was essentially absent in TLR2-deficient macrophages. Similarly, human TLR2 mediated M. leprae-dependent activation of NF-{kappa}B in transfected Chinese hamster ovary and human embryonic kidney 293 cells, with enhancement of this signaling in the presence of CD14. In contrast, activation of NF-{kappa}B by human TLR2Arg677Trp was abolished in response to M. leprae and Mycobacterium tuberculosis. The impaired function of this TLR2 variant provides a molecular mechanism for the poor cellular immune response associated with lepromatous leprosy and may have important implications for understanding the pathogenesis of other mycobacterial infections.




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