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© Artur Scherf
Scanning Electron Microscopy of Red Blood Cell infected by Plasmodium falciparum.
Publication : The Journal of experimental medicine

Critical role of the neutrophil-associated high-affinity receptor for IgE in the pathogenesis of experimental cerebral malaria

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of experimental medicine - 03 Oct 2011

Porcherie A, Mathieu C, Peronet R, Schneider E, Claver J, Commere PH, Kiefer-Biasizzo H, Karasuyama H, Milon G, Dy M, Kinet JP, Louis J, Blank U, Mécheri S

Link to Pubmed [PMID] – 21967768

J. Exp. Med. 2011 Oct;208(11):2225-36

The role of the IgE-FcεRI complex in malaria severity in Plasmodium falciparum-hosting patients is unknown. We demonstrate that mice genetically deficient for the high-affinity receptor for IgE (FcεRIα-KO) or for IgE (IgE-KO) are less susceptible to experimental cerebral malaria (ECM) after infection with Plasmodium berghei (PbANKA). Mast cells and basophils, which are the classical IgE-expressing effector cells, are not involved in disease as mast cell-deficient and basophil-depleted mice developed a disease similar to wild-type mice. However, we show the emergence of an FcεRI(+) neutrophil population, which is not observed in mice hosting a non-ECM-inducing PbNK65 parasite strain. Depletion of this FcεRI(+) neutrophil population prevents ECM, whereas transfer of this population into FcεRIα-KO mice restores ECM susceptibility. FcεRI(+) neutrophils preferentially home to the brain and induce elevated levels of proinflammatory cytokines. These data define a new pathogenic mechanism of ECM and implicate an FcεRI-expressing neutrophil subpopulation in malaria disease severity.

http://www.ncbi.nlm.nih.gov/pubmed/21967768