Abstract
Little is known of the direct microbicidal activity of T cells in leprosy, so a lipopeptide consisting of the N-terminal 13 amino acids lipopeptide (LipoK) of a 33-kD lipoprotein of Mycobacterium leprae, was synthesized. LipoK activated M. leprae infected human dendritic cells (DCs) to induce the production of IL-12. These activated DCs stimulated autologous CD4+ or CD8+ T cells towards type 1 immune response by inducing interferon-gamma secretion. T cell proliferation was also evident from the CFSE labeling of target CD4+ or CD8+ T cells. The direct microbicidal activity of T cells in the control of M. leprae multiplication is not well understood. The present study showed significant production of granulysin, granzyme B and perforin from these activated CD4+ and CD8+ T cells when stimulated with LipoK activated, M. leprae infected DCs. Assessment of the viability of M. leprae in DCs indicated LipoK mediated T cell-dependent killing of M. leprae. Remarkably, granulysin as well as granzyme B could directly kill M. leprae in vitro. Our results provide evidence that LipoK could facilitate M. leprae killing through the production of effector molecules granulysin and granzyme B in T cells.
Highlights
The introduction of multidrug therapy in 1982 and the WHO campaign for the ‘elimination of leprosy as a public health problem’, have contributed greatly to the decrease in the prevalence rate over the past three decades
We observed that LipoK (Mycobacterium leprae lipopeptide with 13 amino acids) is capable of inducing a good immune response in M. leprae infected human dendritic cells (DCs)
LipoK activated human dendritic cells We investigated the effect of LipoK stimulation on human monocyte derived DCs
Summary
The introduction of multidrug therapy in 1982 and the WHO campaign for the ‘elimination of leprosy as a public health problem’, have contributed greatly to the decrease in the prevalence rate over the past three decades. Leprosy still remains to be a public health problem in some countries, and the number of new cases detected during the last three years, remain steady [1]. Patients with the tuberculoid form of the disease are relatively resistant to the bacilli, so that few, if any, demonstrable bacilli are seen in the lesions [2,3]. For patients with abundant bacilli, whose lesions are characterized by type-2 cytokines, there is a need to up-regulate the T-cell mediated type 1 immune responses, by immunotherapeutic means to kill the bacilli
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