| First Author | Porcherie A | Year | 2011 |
| Journal | J Exp Med | Volume | 208 |
| Issue | 11 | Pages | 2225-36 |
| PubMed ID | 21967768 | Mgi Jnum | J:178860 |
| Mgi Id | MGI:5300426 | Doi | 10.1084/jem.20110845 |
| Citation | Porcherie A, et al. (2011) Critical role of the neutrophil-associated high-affinity receptor for IgE in the pathogenesis of experimental cerebral malaria. J Exp Med 208(11):2225-36 |
| abstractText | The role of the IgE-FcepsilonRI complex in malaria severity in Plasmodium falciparum-hosting patients is unknown. We demonstrate that mice genetically deficient for the high-affinity receptor for IgE (FcepsilonRIalpha-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 FcepsilonRI(+) neutrophil population, which is not observed in mice hosting a non-ECM-inducing PbNK65 parasite strain. Depletion of this FcepsilonRI(+) neutrophil population prevents ECM, whereas transfer of this population into FcepsilonRIalpha-KO mice restores ECM susceptibility. FcepsilonRI(+) 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 FcepsilonRI-expressing neutrophil subpopulation in malaria disease severity. |
