Leukocyte subsets in the granulomatous response produced after inoculation with Mycobacterium leprae-BCG in lepromatous patients.

Leukocyte subsets present in the granulomatous response produced after the inoculation of a mixture of Mycobacterium leprae and BCG in lepromatous leprosy patients were characterized in situ using monoclonal antibodies and an immunoperoxidase technique. The granuloma produced after M. leprae-BCG inoculation showed a distribution pattern similar to tuberculoid granulomas. T lymphocytes bearing the CD8 phenotype (T cytotoxic/suppressor) were sequestered to the periphery of the epithelioid tubercles and T helper-inducer CD4+ lymphocytes were distributed throughout the infiltrate. Langerhans cells CD1+ were increased in the epidermis, and in dermis they were localized mainly in the mantle surrounding the granuloma. Most of the dermal infiltrate produced after the inoculation or M. leprae-BCG expresses the HLA-DR antigen. Similarly, most keratinocytes were also positive to this MHC antigen. The granulomatous response to BCG was similar to the inoculation of a mixture of M. leprae-BCG, however acid-fast bacilla were still present. The inoculation of M. leprae produced a macrophage granuloma with no clearing of the bacilla which resembles the lepromatous leprosy granuloma.

In situ characterization of the cellular immune response in American cutaneous leishmaniasis.

American cutaneous leishmaniasis is a spectrum of granulomatous disease caused by related species of an intracellular parasite. The host response in localized cutaneous leishmaniasis (LCL) is effective in that few organisms can be found in tissue lesions. In contrast, diffuse cutaneous leishmaniasis (DCL) patients mount a poor response with numerous parasites present in multiple skin lesions. Immunopathological correlates were sought in LCL and DCL with immunoperoxidase techniques using monoclonal antibodies directed against T lymphocyte subpopulations and interleukin-2 in tissue lesions. Both LCL and DCL granulomas showed a mixture of T lymphocyte subpopulations with the ratio of helper:suppressor phenotypes less than one. This ratio and localization of cells is more similar to the ineffective lepromatous leprosy granuloma than the effective tuberculoid leprosy granuloma. In contrast, interleukin-2 was identified in equivalent numbers of cells in LCL and tuberculoid leprosy, an order of magnitude greater than DCL and lepromatous leprosy lesions. Cells expressing Tac, the receptor for interleukin-2, were present in approximately equal numbers in all disorders. The immunological effectiveness of granulomas appear to related less to the numbers and location of T cell phenotypes than to the functional aspects of these cells, particularly the ability to generate lymphokines.