[The macrophage: chief of tuberculosis immune response].
With nearly eight million new cases each year and two million deaths, tuberculosis (TB) remains a major health problem worldwide. The limited protection afforded by the only available vaccine, Bacille Calmette-Guerin BCG, and the emergence of multi-resistant strains to antibiotics along with the advent of AIDS, are three main causes that contributed to the increase of TB incidence during the last decade. The World Health Organization (WHO) estimates between 2000 and 2020, nearly one billion people will be newly infected with Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, and 200 millions of them will develop the disease, of which 35 million will die if there is no improvement in controlling infection. Such improvement requires an increase in our knowledge of the fundamental biology of this very complex disease and in particular a better understanding and characterization of the types of interactions between mycobacteria and the immune system. The alveolar macrophage (MØA), the first immunological barrier that opposes the mycobacteria, plays a key role in the evolution of infection. In addition to the recognition and immediate elimination of the bacteria by phagocytosis and secretion of microbicidal products, MØA is extremely important in orchestrating the immune response and the establishment of a specific response provided by T cells. This review summarizes the state of our knowledge about the mechanisms deployed by the macrophage to contain Mtb infection with a focus on apoptosis as an innate immune response against this pathogen. We also describe the mechanisms developed by Mtb, during its coexistence with humans, in order to escape the macrophage response.
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D006801:Humans; D008262:Macrophage Activation; D008264:Macrophages / Q000378:metabolism*; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D010587:Phagocytosis; D014376:Tuberculosis / Q000276:immunology*