@article{21301,
  keywords = {Adaptive Immunity, Antigens, Bacterial, Complement Activation, Complement C3, Dendritic Cells, Glycolipids, Humans, Interleukin-10, leprosy, Mycobacterium leprae, T-Lymphocytes},
  author = {Callegaro-Filho D and Shrestha N and Burdick A and Haslett P},
  title = {A potential role for complement in immune evasion by Mycobacterium leprae.},
  abstract = {<p>Lepromatous leprosy is a model of immune evasion wherein pathogen-specific IL-10-secreting T cells and concomitant failure of Th-1 immunity permit uncontrolled proliferation of the intracellular pathogen, Mycobacterium leprae (M. leprae). The mechanism of this immune escape is unknown. Here, the authors report that phenolic glycolipid-1 (PGL-1), a major and distinguishing feature of the M. leprae cell wall, is expressed in the cell membrane of M. leprae-infected human dendritic cells, where it can activate complement in human serum. The authors demonstrate that PGL-1 and the C3 component of complement colocalize in lipid rafts in the dendritic cell membrane, and enter the immune synapse upon co-culture of M. leprae-infected DCs and T cells. Hence, activated C3 is strategically located to costimulate naïve T cells via the complement regulatory protein, CD46, a process known to stimulate the differentiation of IL-10-secreting regulatory T cells. These observations suggest a potential novel mechanism of immune evasion, wherein M. leprae may subvert host natural immunity to provoke an adaptive response that favors bacillary survival.</p>},
  year = {2010},
  journal = {Journal of drugs in dermatology : JDD},
  volume = {9},
  pages = {1373-82},
  month = {2010 Nov},
  issn = {1545-9616},
  doi = {10.2340/16501977-0625},
  language = {eng},
}