Systemic Mycobacterium kansasii infection and regulation of the alloantigenic response.

Specific-pathogen-free B6D2 F1 hybrid mice were infected intravenously with 10(7) to 10(8) viable Mycobacterium kansasii cells. The growth of the five test strains in vivo was correlated with the level of delayed hypersensitivity to a cytoplasmic protein antigen injected into the footpad. M. kansasii TMC no. 1201 and 1203 gave rise to persisting systemic infections with an early delayed hypersensitivity response (day 7) followed by a profound anergy to the cytoplasmic protein antigen injections. Strains 1204, 1214, and 1217 declined in viability relatively rapidly and failed to induce detectable levels of delayed hypersensitivity. Spleens harvested from mice infected 20 to 30 days earlier with 10(8) M. kansasii 1203 cells contained a T-cell subpopulation capable of suppressing mixed lymphocyte reactions between normal B6D2 and C3H(He) cells. On the other hand, splenic T-cells taken from M. kansasii 1214-infected mice enhanced, rather than suppressed, the indicator mixed lymphocyte reactions. The kinetics of stimulator-suppressor T-cell production within the spleens of the heavily infected mice differed as the two contrasting M. kansasii infections progressed. Such cellular interactions could well be responsible for the observed persistence of the systemic M. kansasii 1203 infection.