Schwann cells are able to present exogenous mycobacterial hsp70 to antigen-specific T lymphocytes.

Peripheral nerves are frequently damaged during infection with Mycobacterium leprae. Although Schwann cells are host for this obligate intracellular parasite, the mechanisms of immunopathology are unresolved. This study examines the ability of Lewis rat Schwann cells to present an exogenous Mycobacterium leprae protein, the heat shock protein 70 (hsp70), to antigen-specific T lymphocytes isolated from the lymph nodes of immunised rats. Secondary reactivation of hsp70-specific T lymphocytes occurred producing an antigen-specific lymphoproliferative response. This was inhibited by monoclonal antibodies against rat major histocompatibility complex (MHC) class II molecules, but not antibodies against MHC class I molecules. Coculture of Schwann cells with the M.leprae hsp70-specific T lymphocytes and antigen (MLrp70) induced the expression of MHC class II molecules on the Schwann cell's surface. Although M.leprae hsp70 is immunodominant in the host response to the bacillus, there is a high degree of homology between human and M.leprae hsp70. The M.leprae hsp70-specific T lymphocytes also recognised human hsp70 presented by Schwann cells confirming that antigenic determinants are conserved between the proteins. The ability of Schwann cells to present protein antigens in an MHC class II-restricted manner, to antigen-specific T lymphocytes involved in surveillance of the peripheral nervous system, may play an important role in the activation of an immunological reaction associated with nerve damage seen in tuberculoid leprosy.