Genetic control of immune responses to the 18-kDa protein of Mycobacterium leprae: Different T H1 subsets may be involved in proliferative and delayed-type hypersensitivity responses

Abstract

In vitro and in vivo responses to the 18-kDa protein of Mycobacterium leprae have been analysed in different strains of mice. Lymphocytes from BALB/cJ (H-2 d), BALB.B (H-2 b), B10.BR (H-2 k), and B10.M (H-2 f) mice primed with 18-kDa protein yielded high T cell proliferative responses, while those from C57BL/10J (H-2 b) mice yielded lower responses. Both H-2 and non-H-2 genes contributed to the magnitude of responsiveness. F 1 mice from high and low responder strains showed high responsiveness to the 18-kDa protein. Supernatants from lymph node cell cultures prepared from 18-kDa protein-immunised BALB/cJ, B10.BR, and C57BL/10J mice contained IL-2 but no IL-4, indicating that activated T cells from both high and low responder mice were of a T H1 phenotype. Cell cultures from low responder C57BL/10J mice produced less IL-2 than those from high responders. The low responsiveness to the 18-kDa protein in proliferative assays might be due to a low frequency of antigen-specific T cells in the C57BL/10J mouse strain. BALB/cJ, C57BL/10J, and F 1 (BALB/cJ X B10.BR) mouse strains were tested for in vivo DTH reactions to the 18-kDa protein. All strains, including C57BL/10J, were high DTH responders. Although DTH effector cells and 18-kDa protein-specific proliferative T cells belong to the T H1 subset, our data comparing high and low responder status indicate that distinct T H1 subpopulations are stimulated in response to the 18-kDa protein of M. leprae.