TY - JOUR KW - Antigens, Bacterial KW - Antigens, Differentiation, T-Lymphocyte KW - CD4-Positive T-Lymphocytes KW - CD8-Positive T-Lymphocytes KW - Cell Proliferation KW - Dendritic Cells KW - Granzymes KW - Humans KW - Interferon-gamma KW - Interleukin-12 KW - Lipopeptides KW - Microbial Viability KW - Mycobacterium leprae KW - Perforin AU - Maeda Y AU - Tamura T AU - Fukutomi Y AU - Mukai T AU - Kai M AU - Makino M AB -

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.

BT - PLoS neglected tropical diseases C1 - http://www.ncbi.nlm.nih.gov/pubmed/22132248?dopt=Abstract C2 - USA CY - San Francisco DA - 2011 Nov DO - 10.1371/journal.pntd.0001401 IS - 11 J2 - PLoS Negl Trop Dis LA - eng N2 -

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.

PB - Public Library of Science PP - San Francisco PY - 2011 EP - e1401 T2 - PLoS neglected tropical diseases TI - A lipopeptide facilitate induction of Mycobacterium leprae killing in host cells. UR - http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0001401 VL - 5 SN - 1935-2735 ER -