Establishment of mouse cell lines expressing Mycobacterium leprae 65 KDa heat shock protein gene.

Abstract

Neurotropism is one of the most important characteristics of Mycobacterium leprae (M. leprae). It is believed that nerve damage of leprosy is caused by various immune mechanisms 1), and so called "autoimmune reaction" is suspected to have one of the role in nerve damage.M. leprae 65 kDa heat-shock protein (hsp65) has noticeable characteristics. Hsp65 is a highly conserved protein2). Itbelongs to the family of groEL proteins3). The amino acid sequence of M. leprae hsp65 shows homology of more than 90% with other mycobacterial hsp65s and shares around 48% amino acid identity with the mammalian mitochondrial P1 or hsp 604). Hsp65 was also reported to be a highly immunogenic protein of M. leprae in both Bcell and T-cell responses5, 6). Recently, many reports have described the relationships between hsp65 and some autoimmune diseases such as Kawasaki disease7), rheumatoid arthritisa8) and so on; the role of hsp65 in immunological disorders may be one of molecular mimicry9). Freedman et al described the expression of hsp 60 and hsp 70 by human glial cells. Such hsps were supposed to be the recognition molecule (s) for γ δT cells which mediated glial cell lysis in uitro 10 There are no providing mechanisms for nerve damage in leprosy just now, but the molecule(s) of hsp65 may at least be the possible candidate as a recognition molecule for γ δT cells generated during M. leprae infection.In this paper we reported stablishment of mouse cell lines showing stable expression of M. leprae hsp65, such cell lines would work as a target cell in cytolysis assay in vitro for cytotoxic T cells and γ δT cells generating during M, leprae infections.