Host Defense Mechanisms Triggered by Microbial Lipoproteins Through Toll-Like Receptors

Author:

Brightbill Hans D.1,Libraty Daniel H.2,Krutzik Stephan R.1,Yang Ruey-Bing3,Belisle John T.4,Bleharski Joshua R.1,Maitland Michael5,Norgard Michael V.6,Plevy Scott E.7,Smale Stephen T.189,Brennan Patrick J.4,Bloom Barry R.510,Godowski Paul J.3,Modlin Robert L.1811

Affiliation:

1. Department of Microbiology and Immunology, and the

2. Infectious Disease, Department of Medicine,

3. Genentech Incorporated, South San Francisco, CA 94080, USA.

4. Department of Microbiology, Colorado State University, Fort Collins, CO 80523, USA.

5. Albert Einstein College of Medicine and Howard Hughes Medical Institute, Bronx, NY 10461, USA.

6. University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.

7. Immunobiology Center, Mount Sinai School of Medicine, New York, NY 10029–6574, USA.

8. Molecular Biology Institute, Divisions of

9. Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Angeles, CA 90095, USA.

10. Office of the Dean, Harvard School of Public Health, Boston, MA 02115, USA.

11. Dermatology and

Abstract

The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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