SUMMARYWe have studied the role of three mouse distinct non-H-2 genes (Bcg, Tbc-1, xid ) in several phenomena of antituberculosis immunity and resistance. On the basis of median survival time (MST) of mice following infection with virulent Mycobacterium tuberculosis H37Rv, Bcg gene did not control resistance to the lethal dose of H37Rv infection in non-vaccinated and Myco. bovis (BCG)-vaccinated mice. However, Bcg r allele, in comparison with Bcg s allele, determined more effective suppression of an early multiplication in spleens of H37Rv mycobacteria after a low dose (5 2 10 4 colony-forming units (CFU)) injection. CBA/N mice, which are not protected efficiently against tuberculous challenge by BCG vaccination, were characterized by a decreased in vitro proliferation of immune lymph node cells, both spontaneous and stimulated with mycobacterial antigens. The decreased proliferation was due to immunosuppression caused by interactions between responding T cells and CBA/N antigen-presenting cells (APC). We have confirmed that the defective response to BCG-vaccination in CBA/N mice is linked with the X-chromosome and thus is presumably determined by the xid gene itself. I/St mice (Tbc-1 s ), supersusceptible to H37Rv infection, were not able to restrict the growth of H37Rv mycobacteria in spleens, even following infection with a low dose (5 2 10 4 ), but restricted the growth of Myco. bovis BCG more effectively than Bcg s mice.

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Immunological memory was reproduced and studied by subcutaneous vaccination of mice with attenuated strain of Mycobacterium bovis. Ionomycin-resistant cells of CBA mice were for the first time isolated from immune cells and studied as memory T-cells. Previously they were described for another experimental model. They are characterized by high expression of CD3, CD4, CD8, CD28, and ~/13-T-cell receptor. The capacity of splenocytes and ionomycin-resistant cells to adoptive transfer of antituberculosis resistance to intact recipients is studied.