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Clinical Microbiology Reviews, April 2002, p. 294-309, Vol. 15, No. 2
0893-8512/02/$04.00+0     DOI: 10.1128/CMR.15.2.294-309.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Innate Immunity to Mycobacterium tuberculosis

Reinout van Crevel,1 Tom H. M. Ottenhoff,2 and Jos W. M. van der Meer1*

Department of Internal Medicine, University Medical Center Nijmegen, Nijmegen,,1 and Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands2

The different manifestations of infection with Mycobacterium tuberculosis reflect the balance between the bacillus and host defense mechanisms. Traditionally, protective immunity to tuberculosis has been ascribed to T-cell-mediated immunity, with CD4+ T cells playing a crucial role. Recent immunological and genetic studies support the long-standing notion that innate immunity is also relevant in tuberculosis. In this review, emphasis is on these natural, innate host defense mechanisms, referring to experimental data (e.g., studies in gene knockout mice) and epidemiological, immunological, and genetic studies in human tuberculosis. The first step in the innate host defense is cellular uptake of M. tuberculosis, which involves different cellular receptors and humoral factors. Toll-like receptors seem to play a crucial role in immune recognition of M. tuberculosis, which is the next step. The subsequent inflammatory response is regulated by production of pro- and anti-inflammatory cytokines and chemokines. Different natural effector mechanisms for killing of M. tuberculosis have now been identified. Finally, the innate host response is necessary for induction of adaptive immunity to M. tuberculosis. These basic mechanisms augment our understanding of disease pathogenesis and clinical course and will be of help in designing adjunctive treatment strategies.

* Corresponding author. Mailing address: Department of Internal Medicine, University Medical Center Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. Phone: 003124-3618819. Fax: 0031-243541734. E-mail: j.vandermeer{at}aig.azn.nl.

Clinical Microbiology Reviews, April 2002, p. 294-309, Vol. 15, No. 2
0893-8512/02/$04.00+0     DOI: 10.1128/CMR.15.2.294-309.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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Copyright © 2002 by the American Society for Microbiology. All rights reserved.