Cell Activation and Apoptosis by Bacterial Lipoproteins Through Toll-like Receptor-2-Reference-Cited by-同舟云学术

Cell Activation and Apoptosis by Bacterial Lipoproteins Through Toll-like Receptor-2

Published:1999-07-30 Issue:5428 Volume:285 Page:736-739
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Aliprantis Antonios O.¹,Yang Ruey-Bing²,Mark Melanie R.²,Suggett Shelly³,Devaux Brigitte³,Radolf Justin D.⁴,Klimpel Gary R.⁵,Godowski Paul²,Zychlinsky Arturo¹

Affiliation:

1. Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.

2. Department of Molecular Biology and

3. Antibody Technology Group, Genentech, South San Francisco, CA 94080, USA.

4. Center for Microbial Pathogenesis, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA.

5. Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.

Abstract

Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor–2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor–κB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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