Host defense against Mycobacterium avium does not have an absolute requirement for major histocompatibility complex class I-restricted T cells

The role of CD8(+) T cells was evaluated in a mouse model of disseminated M ycobacterium avium infection. C57BL/6J and C57BL/6J beta(2)(-/-) (beta(2)(- /-)) mice were infected intravenously, and the number of viable bacteria in each liver and spleen was determined. No significant difference between th e number of bacteria in the two strains of mice was observed at 2, 4, 6, an d 8 weeks after infection. Histopathological examination of granulomas from C57BL/6J and beta(2)(-/-) mice did not show any difference either in the n umber of organisms per granuloma or in the size of the granulomas, Investig ation of the cytokine profile in the spleen demonstrated that the beta(2)(- /-) strain of mice produced a significantly lower amount of gamma interfero n at 8 weeks after infection and significantly increased concentrations of tumor necrosis factor alpha compared with that from the wild-type mouse. In terleukin-12 and transforming growth factor beta(1) levels did not differ b etween the two strains of mice at 2, 4, 6, and 8 weeks. Although previous w ork had found that host response against Mycobacterium tuberculosis involve s major histocompatibility complex class I-restricted T cells, our results indicate that chronic deficiency of CD8(+) T cells does not lead to a diffe rent expression of the disease and that if CD8(+) T cells are involved in t he host response, their function can be assumed by other immune cells.