Detecção de TGF-β1 em lesões cutâneas de diferentes formas clínicas de hanseníase

• Ano de defesa: 1995
• Autor(a) principal: Goulart, Isabela Maria Bernardes
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Uberlândia; Brasil; Programa de Pós-graduação em Imunologia e Parasitologia Aplicadas
• Palavras-chave em Português: Estudos imunohistoquímicos; Citocina; Lesões cutâneas; Hanseníase; CNPQ::CIENCIAS BIOLOGICAS::IMUNOLOGIA; Imunologia; Parasitologia - Pesquisa; Lesões dos tecidos moles
• Link de acesso: https://repositorio.ufu.br/handle/123456789/27645; http://doi.org/10.14393/ufu.di.1995.7

Immunohistochemical studies were performed to determine the presence and distribution of the polypeptide TGF-p 1, a cytokine with macrophage suppressing activity, in skin biopsies from 41 patients with different clinicai forms of leprosy. It was used an anti-TGF-pi polyclonal antibody and the avidin-biotin-peroxidase (ABC-Complex) method. The results demonstrated that the lesions of the lepromatous and borderline-lepromatous forms presented intense cytoplasm staining for TGF-p 1 in the cells of the dermal infiltrate. The reaction in the cells of granulomas from borderline cases was of moderate intensity, whereas in the tuberculoid and borderline-tuberculoid forms there was no detectable immunoreaction in granuloma cells. Considering that in the lepromatous leprosy form M. leprae multiplies in the cytoplasm of macrophages and the lesions are difíuse and consisted of cell with no morphological differentiation cells and functional inactivity, we believed that these alterations may be explained at least in part by the presence of TGF-p 1 in the dermal infiltrate, contributing to the no granulomatous lesion formation, and blocking the microbicity activity. Production of the cytokine may be induced by the presence of the bacillus itself and of its constituents, causing a mechanism of parasite evasion. Simiiarly, the absence of TGF-p 1 in tuberculoid and borderline-tuberculoid leprosy may explain the exacerbation of the specifíc immune response to the M. leprae, determining the intense differentiation of macrophage cells with the formation of well defíned epitheloid granulomas capable of eliminating most of the bacilli.