Chapter category: Bacterial Virulence
Immune Recognition of the Mycobacterial Cell Wall
Intracellular Pathogens in Membrane Interactions and Vacuole Biogenesis
Edited by: Jean-Pierre GorvelISBN: 0-306-47833-1
» Get more information about this book at landesbioscience.com «
Chapter authors:
Steven A. Porcelli and Gurdyal S. Besra
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Mycobacteria are extraordinarily successful pathogens with a remarkable ability to persist within animal tissues even in the presence of an intact immune system. Pathogenic mycobacterial species are predominantly intracellular parasites that replicate within cells of their animal hosts, thus sequestering themselves in an environment that is protected from many of the immune mechanisms that normally eliminate bacterial invaders.1 In the case of M. tuberculosis, the major host cell type infected is the macrophage. Following receptor mediated binding to the macrophage, M. tuberculosis bacilli are endocytosed and delivered to an early endosomal compartment, which then becomes modified into a stable intracellular vesicle that is typically referred to as the mycobacterial phagosome.2 In this location, the bacillus is protected from the actions of neutralizing or opsonizing antibodies and complement, and the major challenge that it faces come from cell-mediated mechanisms of immunity that detect signals originating from infected cells.
Given the important role of cell-mediated immunity in generating protective responses against mycobacteria, it is not surprising that the vertebrate immune system has evolved a variety of mechanisms that stimulate macrophages and lymphocytes in response to infection by these organisms. In the case of macrophages and other myeloid lineage cells, initial contact with M. tuberculosis leads to cellular activation and the rapid production of cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor a (TNFa) which initiate inflammatory cascades, and also to the synthesis of reactive oxygen and reactive nitrogen intermediates that can mediate bactericidal effects.1 T lymphocytes recognize specific antigens of M. tuberculosis and provide a source of interferon-g (IFNg) and other cytokines that are critical to the activation of macrophages. In addition, T lymphocytes have been shown to be capable of directly attacking mycobacteria through their secretion of bactericidal granule components.3 Yet in spite of all this immunological artillery, mycobacteria are difficult or perhaps impossible for the immune system to completely eliminate. Many factors, still mostly poorly characterized or unknown, are likely to contribute to the virulence and persistence of Mycobacterium tuberculosis and other pathogenic mycobacteria. However, a major key to the success of these organisms as pathogens is likely to be their unusual cell wall structure and its many interactions with the immune system.
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