After a brief review of the present knowledge about cell mediated immunity mechanisms involved in controlling mycobacterial diseases, variations of the immune responses to mycobacterial diseases in man and in experimental animals models are described. Related factors involved in the variations of the BCG vaccination effectiveness against human tuberculosis are presented according to present hypotheses on varying potency of BCG strains and influence of previous sensitization with non tuberculous mycobacteria. Also new hypotheses concerning qualitative differences in immune responses to mycobacteria in humans are discussed in association with information suggesting that tuberculosis, as other granulomatous chronic infectious diseases, is a disease in which an immune spectrum can be described with a significant modulation of T and B lymphocyte mediated responses. Evidence obtained in murine experimental models, using BCG infection in inbred and recombinant mice, demonstrated the existence of at least two genes which are able to control the induction and expression of CMI after mycobacterial infection. One of them, being not linked with the major histocompatibility complex gene (non H2), controls the natural non specific activity of the mononuclear phagocytic system and the other, linked with H2 complex, is able to modulate the level of CMI in responsive mice. Collective or individual antituberculosis strategies must be reconsidered following this finding.