Our understanding of how the host immune response kills Plasmodium, the causative agent of malaria, is limited and controversial. One widely held belief is that reactive oxygen species are crucial for controlling parasite replication. One of the hallmarks of blood-stage malaria is the cyclic rupture of erythrocytes by the parasite, which releases free hemoglobin into the circulation. We propose that this free hemoglobin, as well as the hemoglobin within the erythrocyte and surrounding the parasite, effectively shields Plasmodium from reactive oxygen species well in excess of those achievable in vivo.
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Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Biochem Plant Pathol, D-85764 Munich, GermanyHelmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Biochem Plant Pathol, D-85764 Munich, Germany
Lindermayr, Christian
Durner, Joerg
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Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Biochem Plant Pathol, D-85764 Munich, Germany
Tech Univ Munich, Lehrstuhl Biochem Pflanzenpathol, D-85354 Freising Weihenstephan, GermanyHelmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Biochem Plant Pathol, D-85764 Munich, Germany
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Univ Sydney, Royal Prince Alfred Hosp, Sydney Canc Ctr, Discipline Med,Melanoma & Skin Canc Res Inst, Sydney, NSW 2006, AustraliaUniv Sydney, Royal Prince Alfred Hosp, Sydney Canc Ctr, Discipline Med,Melanoma & Skin Canc Res Inst, Sydney, NSW 2006, Australia
Russo, P. A. J.
Halliday, G. M.
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Univ Sydney, Royal Prince Alfred Hosp, Sydney Canc Ctr, Discipline Med,Melanoma & Skin Canc Res Inst, Sydney, NSW 2006, AustraliaUniv Sydney, Royal Prince Alfred Hosp, Sydney Canc Ctr, Discipline Med,Melanoma & Skin Canc Res Inst, Sydney, NSW 2006, Australia