Abstract
Tuberculosis (TB) is a leading cause worldwide of human mortality attributable to a single infectious agent; nevertheless, the infection of human organism with Mycobacterium tuberculosis (Mtb) doesn’t lead to disease obligatory, by all means. Recent studies have revealed numerous polymorphisms implicated in host susceptibility to TB. Human organism may have an innate resistance to MTB. A hallmark of Mtb infection is the ability of most (90- 95%) healthy adults to control infection through acquired immunity, in which antigen specific T cells and macrophages arrest growth of Mtb bacilli and maintain control over persistent bacilli. Mtb induces vigorous immune responses, yet evades host immunity, persisting within phagosomes of the infected macrophages. Each stage of the host response to Mtb is under genetic control, including the initial encounter with MTB by macrophages, epithelial cells and dendritic cells in the lung, induction of the inductive T cell response, and killing by activated macrophages within granulomas. Thus there is an innate resistance of the human organism to Mtb - and it is a main reason why TB, potentially lethal disease, doesn’t destroy all mankind. Mtb itself stimulates acquired response on TB that improves the resistance of the human organism. Special vaccines increase this resistance too. Medical science may help to reinforce both innate and acquired response on TB, nevertheless, genetical predisposition plays important role
Highlights
Tuberculosis (TB) is a leading cause worldwide of human mortality attributable to a single infectious agent [1]; the infection of human organism with Mycobacterium tuberculosis (Mtb) doesn’t lead to disease obligatory, by all means
Gene expression profiles in Mtb-stimulated and unstimulated macrophages was compared and identified 1,608 and 199 genes that were differentially expressed by >2- and >5-fold, respectively. These results suggest that genome-wide studies can provide an unbiased method to identify critical macrophage response genes that are associated with different clinical outcomes and that variation in innate immune response genes regulate susceptibility to TB [7]
Phagocytosed Mtb either multiply inside the endocytic compartment of mononuclear phagocytes or they are destroyed by the host cell, so TB is controlled by the cellular immune response
Summary
Tuberculosis (TB) is a leading cause worldwide of human mortality attributable to a single infectious agent [1]; the infection of human organism with Mycobacterium tuberculosis (Mtb) doesn’t lead to disease obligatory, by all means. Between 10 December 1929 and 30 April 1930, 251 infants born in the old Hanseatic town of Lubeck received three doses of BCG vaccine by the mouth during the first ten days of life. Of these 251, 72 died of TB, most of them in two to five months and all but one before the end of the first year. Mtb infected all children– and some of them died, some of them–got sick with clinical TB, and 17.5% remained healthy, because they had good innate resistance to TB. A diverse T cell response allows the host to recognize a wider range of mycobacterial antigens presented by different families of antigen-presenting molecules, and greater ability to detect the pathogen [3]
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