Induction of Direct Antimicrobial Activity Through Mammalian Toll-Like Receptors-Reference-Cited by-同舟云学术

Induction of Direct Antimicrobial Activity Through Mammalian Toll-Like Receptors

Published:2001-02-23 Issue:5508 Volume:291 Page:1544-1547
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Thoma-Uszynski Sybille¹,Stenger Steffen²,Takeuchi Osamu³,Ochoa Maria Teresa¹,Engele Matthias²,Sieling Peter A.¹,Barnes Peter F.⁴,Röllinghoff Martin²,Bölcskei Pal L.⁵,Wagner Manfred⁵,Akira Shizuo³,Norgard Michael V.⁶,Belisle John T.⁷,Godowski Paul J.⁸,Bloom Barry R.⁹,Modlin Robert L.¹

Affiliation:

1. Division of Dermatology, Department of Microbiology and Immunology and Molecular Biology Institute, UCLA School of Medicine, Los Angeles, CA 90095, USA.

2. Institute for Clinical Microbiology, Immunology and Hygiene, Universität Erlangen, 91054 Erlangen, Germany.

3. Department of Host Defense, Osaka University, Osaka, Japan.

4. Center for Pulmonary and Infectious Disease Control, Departments of Medicine, Cell Biology, and Immunology, University of Texas Health Center, Tyler, TX 75708–3154, USA.

5. Klinikum Nürnberg, Medical Clinic 3, 90419 Nürnberg, Germany.

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

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

8. Department of Molecular Biology, Genentech, South San Francisco, CA 94080, USA.

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

Abstract

The mammalian innate immune system retains from Drosophila a family of homologous Toll-like receptors (TLRs) that mediate responses to microbial ligands. Here, we show that TLR2 activation leads to killing of intracellular Mycobacterium tuberculosis in both mouse and human macrophages, through distinct mechanisms. In mouse macrophages, bacterial lipoprotein activation of TLR2 leads to a nitric oxide–dependent killing of intracellular tubercle bacilli, but in human monocytes and alveolar macrophages, this pathway was nitric oxide–independent. Thus, mammalian TLRs respond (as Drosophila Toll receptors do) to microbial ligands and also have the ability to activate antimicrobial effector pathways at the site of infection.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference30 articles.

1. The Dorsoventral Regulatory Gene Cassette spätzle/Toll/cactus Controls the Potent Antifungal Response in Drosophila Adults

2. Drosophila host defense: Differential induction of antimicrobial peptide genes after infection by various classes of microorganisms

3. Phylogenetic Perspectives in Innate Immunity

4. A human homologue of the Drosophila Toll protein signals activation of adaptive immunity

5. Toll-like receptor-2 mediates lipopolysaccharide-induced cellular signalling

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