@article{fdi:010053886,
  title = {{N}rf2, a {PPAR} gamma alternative pathway to promote {CD}36 expression on inflammatory macrophages : implication for malaria},
  author = {{O}lagnier, {D}. and {L}avergne, {R}. {A}. and {M}eunier, {E}. and {L}efevre, {L}. and {D}ardenne, {C}. and {A}ubouy, {A}gn{\`e}s and {B}enoit-{V}ical, {F}. and {R}yffel, {B}. and {C}oste, {A}. and {B}erry, {A}. and {P}ipy, {B}.},
  editor = {},
  language = {{ENG}},
  abstract = {{CD}36 is the major receptor mediating nonopsonic phagocytosis of {P}lasmodium falciparum-parasitized erythrocytes by macrophages. {I}ts expression on macrophages is mainly controlled by the nuclear receptor {PPAR} gamma. {H}ere, we demonstrate that inflammatory processes negatively regulate {CD}36 expression on human and murine macrophages, and hence decrease {P}lasmodium clearance directly favoring the worsening of malaria infection. {T}his {CD}36 downregulation in inflammatory conditions is associated with a failure in the expression and activation of {PPAR} gamma. {I}nterestingly, using si{RNA} mediating knock down of {N}rf2 in macrophages or {N}rf2- and {PPAR} gamma-deficient macrophages, we establish that in inflammatory conditions, the {N}rf2 transcription factor controls {CD}36 expression independently of {PPAR} gamma. {I}n these conditions, {N}rf2 activators, but not {PPAR} gamma ligands, enhance {CD}36 expression and {CD}36-mediated {P}lasmodium phagocytosis. {T}hese results were confirmed in human macrophages and in vivo where only {N}rf2 activators improve the outcome of severe malaria. {C}ollectively, this report highlights that the {N}rf2 transcription factor could be an alternative target to {PPAR} gamma in the control of severe malaria through parasite clearance.},
  keywords = {},
  booktitle = {},
  journal = {{P}los {P}athogens},
  volume = {7},
  numero = {9},
  pages = {e1002254},
  ISSN = {1553-7366},
  year = {2011},
  DOI = {10.1371/journal.ppat.1002254},
  URL = {https://www.documentation.ird.fr/hor/fdi:010053886},
}