Leprosy is a chronic infectious disease of the skin and peripheral nerves caused by Mycobacterium leprae. This bacillus is obligate intracellular parasite with tropism for Schwann cells and macrophages, whose optimal growth occurs at 27ºC - 30ºC. Based on clinical and histopathological characteristics, leprosy can be classified in two polar forms (tuberculoid and lepromatous), beyond borderline forms and leprosy reactions. In this context, immunologic response has a fundamental role in determination of disease pathogeneses, once it is observed influence of Th1 and Th2 subpopulation in leprosy immunopathogenesis, highlighting Th1 patterns in tuberculoid polo and Th2 in lepromatous polo. Additionally, recent studies have reported the involvement of other T cells subpopulations on leprosy pathogenesis, such as regulatory T cells and Th17. In relation to subpopulations that may be involved in immunoregulation of infectious diseases, recently, B cells have occupied a prominent role. Previously these cells were seen only as antibody producing, but recent studies have shown that they can produce cytokines, similarly to T cell, allowing their subdivision into B cells and regulatory effector B cells (Breg). Considering the importance of B cells in leprosy, especially in the lepromatous polo (VV), since this polo is mainly characterized by a humoral immune response, and before the new functions and subtypes of these cells, this project aims to assess the influence of B cells in experimental leprosy (according to Shepard's technique), specifically in response to M. leprae inoculation assessed by bacillary multiplication, as well as by histopathological characteristics of sites of bacillary multiplication (foodpad), by comparative analysis of wild-type mice (C57BL/6) and B cells knockout.
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