Mecanismos imunitarios nas infeccoes por micobacterias: actividade dos fagocitos profissionais e sua regulacao pelo linfocito T

Abstract

Mycobacterial infections still are major problems in Public Health. Here we studied some parameters of the immunity to mycobacterial infections using the mouse model. We found the involvement of neutrophils in the chronic immunity response to mycobacteria. The recruitment of neutrophils was genetically determined and was mediated by the immune system, namely by the T cells and macrophages. We identified gamma interferon and macrophage inflammatory proteins (MIP) 1 and 2 as molecular mediators of the immune mobilization of neutrophils in mycobacteria-infected animals. The neutrophil may participate in the resistance mechanisms against mycobacteria by cooperating with the macrophage. We identified the Bcg gene as the major determinant of innate resistance to Mycobacterium avium infections in mice. The resident macrophage is the cellular mediator of such innate resistance. The antimycobacterial activity of the macrophage was modulated by T cells in different ways according to the mouse strain and the M. avium isolate. Gamm interferon, tumor necrosis factor, macrophage-granulocyte colony-stimulating factor and interleukin-5 seemed to be involved in innate and acquired resistance to M. avium. The effector mechanism of the macrophage responsible for its antimycobacterial activity does not seem to involve O_2 or nitrogen radicals but rather the vacuolar acidification of the infected macrophagesAvailable from Fundacao para a Ciencia e a Tecnologia, Servico de Informacao e Documentacao, Av. D. Carlos I, 126, 1200 Lisboa / FCT - Fundação para o Ciência e a TecnologiaSIGLEPTPortuga