@article{22261, keywords = {Antigens, Bacterial, Antigens, Differentiation, T-Lymphocyte, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cell Proliferation, Dendritic Cells, Granzymes, Humans, Interferon-gamma, Interleukin-12, Lipopeptides, Microbial Viability, Mycobacterium leprae, Perforin}, author = {Maeda Y and Tamura T and Fukutomi Y and Mukai T and Kai M and Makino M}, title = {A lipopeptide facilitate induction of Mycobacterium leprae killing in host cells.}, 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.
}, year = {2011}, journal = {PLoS neglected tropical diseases}, volume = {5}, pages = {e1401}, month = {2011 Nov}, publisher = {Public Library of Science}, address = {San Francisco}, issn = {1935-2735}, url = {http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0001401}, doi = {10.1371/journal.pntd.0001401}, language = {eng}, }