The objective of this research is to acquire a better insight of the issue of TB vaccination. The research demonstrates a long history of search for a protective vaccine against tuberculosis and evaluates the problem of complications of BCG vaccination…
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From this research it is clear that all people have natural immunity to tuberculosis. The attempts to find a correlation between sensitivity to tuberculosis and HLA phenotype have produced conflicting results. Although sensitivity to tuberculosis is associated with race, the evidence is largely unconvincing. Age is an important determinant of natural resistance to tuberculosis. Although there is no specific data concerning the relationship of nutritional status and immunity against tuberculosis, it is clear that malnutrition and tuberculosis are related in some way. Primary tuberculous infection is associated with the development of acquired immunity. Tuberculosis which is caused by exogenous reinfection in North America and Europe are rare. Much more often it is registered among the population with a high incidence of tuberculosis, where there is a high risk of reinfection. It would be appropriate to note that the immune system in the classic sense of the word means resistance to infection, whereas hypersensitive means a state of the damaged host's reactivity. In this sense, immunity may be the result of infection caused by other mycobacteria, or the result of vaccination of bacillus Calmette-Guerin (BCG), or the result of natural infection with mycobacteria, which common in the environment. This acquired non-specific immunity can be regarded as a reflection of the primary activation of macrophages. (Chan, 2000, 134) Topic 1. M Tuberculosis Antigen-specific immunity is mediated by T-lymphocytes and can be adapted by them. Antigen-specific immunity is strongly correlated with delayed-type hypersensitivity. It can act as an independent factor, but it is believed that functional expression of cellular hypersensitivity is the most efficient. Tuberculin sensitivity is antigen-specific in nature and develops after the primary infection. It is directed mainly against protein antigens. Mycobacterial antigens are the subject of diverse immunochemical studies. (Smith, 2005). It is quite clear that there is no single dominant antigen, and in any microorganism which is artificially infected or sensitized hypersensitivity to the set of mycobacterial proteins develops. Tuberculin purified protein derivative (PPD) is antigen preparation which is most often used in clinical and epidemiological practice in order to identify the tuberculin hypersensitivity and it is a mixture of crude largely denatured antigens and poorly reflects the character of the natural antigens. (Brennan, 2009, 335) In the case of infection in organism the protein antigen mycobacteria are always present in association with this set of adjuvants. In vitro studies have shown that the purified arabynogalactan is a potent immunosuppressive agent. (Chan, 2000, 134) The recognition of antigen which is sensitized by macro-processing is accompanied by macrophages and it depends on the expression of macrophages on their surface of antigen-specific epitopes associated with the Ia-antigen gene product of histocompatibility. This complex is recognized by specific T lymphocytes. For the development of the response of T lymphocytes to antigen presentation also requires macrophage synthesis and secretion of interleukin-1. (Chan, 2000, 137) The immunoreactive cells secrete mediators that can cause activation of macrophages. The macrophages as the main effectors cells of tuberculin hypersensitivity. The peripheral blood monocytes of TB patients have some properties which are the characteristic of activated macrophages, including enhanced activity against hecsomonophosphatus, increased ability to to the surface adhesion, expression of specific membrane structures and increased bactericidal activity. However in some cases of tuberculosis it is possible to observe the deviation from the state of hypersensivity (Chan, 2000, 137). Such cases formed the basis for the assumption that TB can develop in the presence of immunological spectrum in the
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