Tuberculin skin reaction is one of phenotypes of the immune responses to mycobacteria, which is mediated by the sensitized T cells and expressed as a delayed-type hyperse nsitivity. In mycobacteria-infected mice, this response is recognized as a footpad reaction specific to PPD. There are high and low responders in this reaction among various strains of mice. The difference in the responsiveness is controlled genetically. High respon siveness is dominant over low responsiveness. The results of linkage test using SWM/Ms, C3H/ He, and their hybrids, showed that this gene links to neither H-2, coat color, norIgh allotype.
Strain differences in the resistance against virulent mycobacterial infection does not coincide with the natural resistance to BCG which is regulated by Ity-Bcg-Lsh gene on chromosome 1. Rather, the acquired immunity is related to delayed-hypersensitivity to BCG, although it is not mapped yet.
Suppression of the immune response to BCG is observed in BCG-low-responder mice. The mechanism was found to be due to the induction of suppressor T cells which inhibit the induction of effector T cells. The surface antigens on macrophages and T cells are necessary to induce suppressor T cells. It seems that the suppressor T cell induction is regulated genetically. However, it is not clear what gene regulates the suppressor T cell induction and how it is related with the gene for delayed-type hypersensitivity.
Genetic analysis of immunity to tuberculosis in human beings is difficult because the population is highly heterogeneous. Statistical analysis in a large scale would be a good way of the study. There is a report that HLA-Bw 15 might be related to tuberculosis, but accumulation of more information is necessary.