Phosphatidylmyo-inositol mannosides

Phosphatidylmyo-inositol Mannosides (PIM) appear to be a glycolipid component of the cell wall of "Mycobacterium tuberculosis". PIM is heavily involved with immune system interaction with "M. tuberculosis", and mice that develop antibodies for this glycolipid are better at sustaining a "M. tuberculosis" infection or defeating it. [Mehta, P. K., and G. K. Khuller. 1988. Protective immunity to experimental tuberculosis by mannophosphoinositides of mycobacteria. Med. Microbiol. Immunol. (Berlin) 177:265–284.] [Singh, A. P., and G. K. Khuller. 1993. Liposomes as a carrier for mannophosphoinositide antigens of mycobacteria. Indian J. Biochem. Biophys. 30:160–165.] This assertion that PIM is a very important glycolipid associated with "M. tuberculosis" goes further and argues that PIM is likely involved with the process by which "M. tuberculosis" subverts the immune system. [Fratti, R. A., J. M. Backer, J. Gruenberg, S. Corvera, and V. Deretic. 2001. Role of phosphatidylinositol 3-kinase and Rab5 effectors in phagosomal biogenesis and mycobacterial phagosome maturation arrest. J. Cell Biol. 154:631–644.] [Kaplan, G., R. R. Gandhi, D. E. Weinstein, W. R. Levis, M. E. Patarroyo, P. J. Brennan, and Z. A. Cohn. 1987. Mycobacterium leprae antigen-induced suppression of T cell proliferation in vitro. J. Immunol. 138:3028–3034.] [Sibley, L. D., L. B. Adams, and J. L. Krahenbuhl. 1990. Inhibition of interferon-gamma-mediated activation in mouse macrophages treated with lipoarabinomannan. Clin. Exp. Immunol. 80:141–148.] [Vergne, I., J. Chua, and V. Deretic. 2003. Tuberculosis toxin blocking phagosome maturation inhibits a novel Ca2!/calmodulin-PI3K hVPS34 cascade. J. Exp. Med. 198:653–659.] [Vergne, I., R. A. Fratti, P. J. Hill, J. Chua, J. Belisle, and V. Deretic. 2004. Mycobacterium tuberculosis phagosome maturation arrest: mycobacterial phosphatidylinositol analog phosphatidylinositol mannoside stimulates early endosomal fusion. Mol. Biol. Cell 15:751–760.]

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