Immune responses to atypical mycobacterial lung infections

Various species of atypical mycobacteria exhibited a wide range of growth patterns in the lung, liver, and spleen of specific pathogen-free B6D2 mice infected with these organisms. The growth varied from rapid elimination (complete avirulence) to a continued persistence in the lung, which eventually resulted in the death of many of the mice. Prior depletion of the T cells of aerogenically challenged mice did not affect the growth characteristics of the organisms within the lungs. Mice infected with Mycobacterium habana developed an early hypersensitivity response to the cytoplasmic protein antigens (CPA) of this organism, and this response was followed by a persistent state of anergy. Mice infected with Mycobacterium simiae failed to develop detectable levels of hypersensitivity at any time during the study. Spleen cells taken from mice infected with M. habana or M. simiae exhibited an early peak in the incorporation of [3H] thymidine after exposure of the cells to the nonspecific T-cell mitogen phytohemagglutinin (PHA). A similar peak occurred when the cells were exposed to the specific mitogen CPA of M. habana. Later in the infection, the anergic spleen cells showed no transformation of lymphocytes after exposure to either PHA or CPA. T-cell-mixing experiments, which were carried out both before and after treatment of suspensions of cells from the anergic spleens with anti-Thy 1.2 antiserum plus complement, indicated the presence of a population of suppressor T cells in the anergic animals.