Mice deficient in CD4 T cells have only transiently diminished levels of IFN-gamma, yet succumb to tuberculosis.

CD4 T cells are important in the protective immune response against tuberculosis. Two mouse models deficient in CD4 T cells were used to examine the mechanism by which these cells participate in protection against Mycobacterium tuberculosis challenge. Transgenic mice deficient in either MHC class II or CD4 molecules demonstrated increased susceptibility to M.

IL-12 increases resistance of BALB/c mice to Mycobacterium tuberculosis infection.

IL-12, a cytokine produced by macrophages and B cells, has recently been found to exert pleiotropic effects on the immune system. When BALB/c mice, a strain highly susceptible to virulent Mycobacterium tuberculosis infection, were given IL-12 at the initiation of infection with M. tuberculosis, their mean survival time doubled from 58 to 112 days.

Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice.

Understanding the immunological mechanisms of protection and pathogenesis in tuberculosis remains problematic. We have examined the extent to which tumor necrosis factor-alpha (TNF alpha) contributes to this disease using murine models in which the action of TNF alpha is inhibited. TNF alpha was neutralized in vivo by monoclonal antibody; in addition, a mouse strain with a disruption in the gene for the 55 kDa TNF receptor was used.

An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection.

Tuberculosis, a major health problem in developing countries, has reemerged in recent years in many industrialized countries. The increased susceptibility of immunocompromised individuals to tuberculosis, and many experimental studies indicate that T cell-mediated immunity plays an important role in resistance. The lymphokine interferon gamma (IFN-gamma) is thought to be a principal mediator of macrophage activation and resistance to intracellular pathogens.