Abstract

One of the most intriguing aspects of leprosy is the close correlation between its clinical and immunological spectrum. There are two polar forms of the disease, tuberculoid and lepromatous leprosy, with a number of intermediate stages. Tuberculoid (TT) or high responder patients usually have only a few, localized lesions with rarely detectable leprosy bacteria. They usually display a strong cell mediated immune response to Mycobacterium leprae. On the other pole of the spectrum are lepromatous (LL) leprosy patients that have numerous diffuse skin lesions with vast numbers of M.leprae organisms residing in unactivated macrophages. Lepromatous leprosy patients typically show a selective T cell nonresponsiveness to antigens of M.leprae, in vivo and in vitro, which is selective because T cell responses to closely related organisms like M.tuberculosis are usually intact. The extraordinary specificity of the defect in T cell reactivity to M.leprae antigens makes lepromatous leprosy a model disease for the study of antigen specific T cell unresponsiveness in man (Bloom and Godal 1983).

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