The Microcirculation in Severe Malaria
Identifieur interne : 001129 ( Istex/Corpus ); précédent : 001128; suivant : 001130The Microcirculation in Severe Malaria
Auteurs : Stephen J. Rogerson ; Georges E. Grau ; Nicholas H. HuntSource :
- Microcirculation [ 1073-9688 ] ; 2004-10-11.
English descriptors
- KwdEn :
- Acad, Adhesion, African children, Aikawa, Berendt, Birth weight, Blood cells, Brain microvessels, Cerebral, Cerebral endothelium, Cerebral malaria, Cerebral vessels, Cerebrospinal fluid, Chondroitin, Chondroitin sulfate, Clinical disease, Coma, Cytoadherence, Cytoadherence characteristics, Cytokine, Dendritic cells, Disease severity, Endothelial, Endothelial cells, Endothelial receptors, Endothelium, Erythrocyte, Experimental murine, Falciparum, Falciparum malaria, Fatal murine, Fibrin deposition, Flow conditions, Grau, Greenwood, Host receptors, Human microvascular, Human placenta, Human studies, Immune, Immunol, Inflammatory, Intercellular, Intercellular adhesion, Intervillous, Intervillous space, Kynurenine pathway, Lancet, Leukocyte, Looareesuwan, Malaria, Malaria infection, Malaria pathogenesis, Malaria pigment, Malarial, Medana, Mediator, Microcirculation, Microvascular, Microvessels, Model systems, Molyneux, Monocyte, Murine, Neuronal damage, Newbold, Nitric, Nitric oxide, Noncerebral malaria, Other receptors, Parasite, Parasitized, Parasitized erythrocytes, Parasitol, Parasitol today, Pathogenesis, Pathol, Pathway, Pfemp1, Placenta, Placental, Placental malaria, Plasmodium, Plasmodium erythrocytes, Plasmodium falciparum, Plasmodium falciparum cytoadherence, Plasmodium falciparum erythrocyte membrane protein, Platelet, Platelet accumulation, Pregnant women, Proc natl acad, Quinolinic acid, Receptor, Reeder, Rogerson, Rosette, Rosetting, Sequestration, Severe falciparum malaria, Severe malaria, Stocker, Sulfate, Trans, Tryptophan metabolism, Tumor necrosis factor, Uninfected erythrocytes, Vascular cell adhesion molecule, Wahlgren.
- Teeft :
- Acad, Adhesion, African children, Aikawa, Berendt, Birth weight, Blood cells, Brain microvessels, Cerebral, Cerebral endothelium, Cerebral malaria, Cerebral vessels, Cerebrospinal fluid, Chondroitin, Chondroitin sulfate, Clinical disease, Coma, Cytoadherence, Cytoadherence characteristics, Cytokine, Dendritic cells, Disease severity, Endothelial, Endothelial cells, Endothelial receptors, Endothelium, Erythrocyte, Experimental murine, Falciparum, Falciparum malaria, Fatal murine, Fibrin deposition, Flow conditions, Grau, Greenwood, Host receptors, Human microvascular, Human placenta, Human studies, Immune, Immunol, Inflammatory, Intercellular, Intercellular adhesion, Intervillous, Intervillous space, Kynurenine pathway, Lancet, Leukocyte, Looareesuwan, Malaria, Malaria infection, Malaria pathogenesis, Malaria pigment, Malarial, Medana, Mediator, Microcirculation, Microvascular, Microvessels, Model systems, Molyneux, Monocyte, Murine, Neuronal damage, Newbold, Nitric, Nitric oxide, Noncerebral malaria, Other receptors, Parasite, Parasitized, Parasitized erythrocytes, Parasitol, Parasitol today, Pathogenesis, Pathol, Pathway, Pfemp1, Placenta, Placental, Placental malaria, Plasmodium, Plasmodium erythrocytes, Plasmodium falciparum, Plasmodium falciparum cytoadherence, Plasmodium falciparum erythrocyte membrane protein, Platelet, Platelet accumulation, Pregnant women, Proc natl acad, Quinolinic acid, Receptor, Reeder, Rogerson, Rosette, Rosetting, Sequestration, Severe falciparum malaria, Severe malaria, Stocker, Sulfate, Trans, Tryptophan metabolism, Tumor necrosis factor, Uninfected erythrocytes, Vascular cell adhesion molecule, Wahlgren.
Abstract
Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of the microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.
Url:
DOI: 10.1080/10739680490503311
Links to Exploration step
ISTEX:5B1AF32532823B4354AF2AB842A41583B83424D1Le document en format XML
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conditions</term><term>Grau</term><term>Greenwood</term><term>Host receptors</term><term>Human microvascular</term><term>Human placenta</term><term>Human studies</term><term>Immune</term><term>Immunol</term><term>Inflammatory</term><term>Intercellular</term><term>Intercellular adhesion</term><term>Intervillous</term><term>Intervillous space</term><term>Kynurenine pathway</term><term>Lancet</term><term>Leukocyte</term><term>Looareesuwan</term><term>Malaria</term><term>Malaria infection</term><term>Malaria pathogenesis</term><term>Malaria pigment</term><term>Malarial</term><term>Medana</term><term>Mediator</term><term>Microcirculation</term><term>Microvascular</term><term>Microvessels</term><term>Model systems</term><term>Molyneux</term><term>Monocyte</term><term>Murine</term><term>Neuronal damage</term><term>Newbold</term><term>Nitric</term><term>Nitric oxide</term><term>Noncerebral malaria</term><term>Other receptors</term><term>Parasite</term><term>Parasitized</term><term>Parasitized erythrocytes</term><term>Parasitol</term><term>Parasitol today</term><term>Pathogenesis</term><term>Pathol</term><term>Pathway</term><term>Pfemp1</term><term>Placenta</term><term>Placental</term><term>Placental malaria</term><term>Plasmodium</term><term>Plasmodium erythrocytes</term><term>Plasmodium falciparum</term><term>Plasmodium falciparum cytoadherence</term><term>Plasmodium falciparum erythrocyte membrane protein</term><term>Platelet</term><term>Platelet accumulation</term><term>Pregnant women</term><term>Proc natl acad</term><term>Quinolinic acid</term><term>Receptor</term><term>Reeder</term><term>Rogerson</term><term>Rosette</term><term>Rosetting</term><term>Sequestration</term><term>Severe falciparum malaria</term><term>Severe malaria</term><term>Stocker</term><term>Sulfate</term><term>Trans</term><term>Tryptophan metabolism</term><term>Tumor necrosis factor</term><term>Uninfected erythrocytes</term><term>Vascular cell adhesion molecule</term><term>Wahlgren</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Acad</term><term>Adhesion</term><term>African children</term><term>Aikawa</term><term>Berendt</term><term>Birth weight</term><term>Blood cells</term><term>Brain microvessels</term><term>Cerebral</term><term>Cerebral endothelium</term><term>Cerebral malaria</term><term>Cerebral vessels</term><term>Cerebrospinal fluid</term><term>Chondroitin</term><term>Chondroitin sulfate</term><term>Clinical disease</term><term>Coma</term><term>Cytoadherence</term><term>Cytoadherence characteristics</term><term>Cytokine</term><term>Dendritic cells</term><term>Disease severity</term><term>Endothelial</term><term>Endothelial cells</term><term>Endothelial receptors</term><term>Endothelium</term><term>Erythrocyte</term><term>Experimental murine</term><term>Falciparum</term><term>Falciparum malaria</term><term>Fatal murine</term><term>Fibrin deposition</term><term>Flow conditions</term><term>Grau</term><term>Greenwood</term><term>Host receptors</term><term>Human microvascular</term><term>Human placenta</term><term>Human studies</term><term>Immune</term><term>Immunol</term><term>Inflammatory</term><term>Intercellular</term><term>Intercellular adhesion</term><term>Intervillous</term><term>Intervillous space</term><term>Kynurenine pathway</term><term>Lancet</term><term>Leukocyte</term><term>Looareesuwan</term><term>Malaria</term><term>Malaria infection</term><term>Malaria pathogenesis</term><term>Malaria pigment</term><term>Malarial</term><term>Medana</term><term>Mediator</term><term>Microcirculation</term><term>Microvascular</term><term>Microvessels</term><term>Model systems</term><term>Molyneux</term><term>Monocyte</term><term>Murine</term><term>Neuronal damage</term><term>Newbold</term><term>Nitric</term><term>Nitric oxide</term><term>Noncerebral malaria</term><term>Other receptors</term><term>Parasite</term><term>Parasitized</term><term>Parasitized erythrocytes</term><term>Parasitol</term><term>Parasitol today</term><term>Pathogenesis</term><term>Pathol</term><term>Pathway</term><term>Pfemp1</term><term>Placenta</term><term>Placental</term><term>Placental malaria</term><term>Plasmodium</term><term>Plasmodium erythrocytes</term><term>Plasmodium falciparum</term><term>Plasmodium falciparum cytoadherence</term><term>Plasmodium falciparum erythrocyte membrane protein</term><term>Platelet</term><term>Platelet accumulation</term><term>Pregnant women</term><term>Proc natl acad</term><term>Quinolinic acid</term><term>Receptor</term><term>Reeder</term><term>Rogerson</term><term>Rosette</term><term>Rosetting</term><term>Sequestration</term><term>Severe falciparum malaria</term><term>Severe malaria</term><term>Stocker</term><term>Sulfate</term><term>Trans</term><term>Tryptophan metabolism</term><term>Tumor necrosis factor</term><term>Uninfected erythrocytes</term><term>Vascular cell adhesion molecule</term><term>Wahlgren</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of the microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>plasmodium</json:string><json:string>erythrocyte</json:string><json:string>falciparum</json:string><json:string>receptor</json:string><json:string>severe malaria</json:string><json:string>platelet</json:string><json:string>malaria</json:string><json:string>monocyte</json:string><json:string>microcirculation</json:string><json:string>murine</json:string><json:string>rogerson</json:string><json:string>cerebral malaria</json:string><json:string>cytoadherence</json:string><json:string>microvascular</json:string><json:string>pfemp1</json:string><json:string>cytokine</json:string><json:string>endothelial</json:string><json:string>grau</json:string><json:string>sequestration</json:string><json:string>plasmodium erythrocytes</json:string><json:string>endothelial cells</json:string><json:string>immunol</json:string><json:string>molyneux</json:string><json:string>adhesion</json:string><json:string>placenta</json:string><json:string>sulfate</json:string><json:string>plasmodium falciparum</json:string><json:string>parasitol</json:string><json:string>chondroitin</json:string><json:string>placental</json:string><json:string>pathol</json:string><json:string>parasite</json:string><json:string>rosetting</json:string><json:string>endothelium</json:string><json:string>looareesuwan</json:string><json:string>pathway</json:string><json:string>lancet</json:string><json:string>intervillous</json:string><json:string>leukocyte</json:string><json:string>chondroitin sulfate</json:string><json:string>pathogenesis</json:string><json:string>microvessels</json:string><json:string>wahlgren</json:string><json:string>mediator</json:string><json:string>coma</json:string><json:string>nitric</json:string><json:string>medana</json:string><json:string>intercellular</json:string><json:string>berendt</json:string><json:string>parasitized</json:string><json:string>acad</json:string><json:string>trans</json:string><json:string>blood cells</json:string><json:string>immune</json:string><json:string>stocker</json:string><json:string>rosette</json:string><json:string>aikawa</json:string><json:string>malarial</json:string><json:string>placental malaria</json:string><json:string>proc natl acad</json:string><json:string>parasitol today</json:string><json:string>intervillous space</json:string><json:string>tumor necrosis factor</json:string><json:string>african children</json:string><json:string>falciparum malaria</json:string><json:string>disease severity</json:string><json:string>uninfected erythrocytes</json:string><json:string>greenwood</json:string><json:string>cerebral vessels</json:string><json:string>platelet accumulation</json:string><json:string>brain microvessels</json:string><json:string>severe falciparum malaria</json:string><json:string>fatal murine</json:string><json:string>intercellular adhesion</json:string><json:string>nitric oxide</json:string><json:string>kynurenine pathway</json:string><json:string>malaria pigment</json:string><json:string>host receptors</json:string><json:string>plasmodium falciparum erythrocyte membrane protein</json:string><json:string>flow conditions</json:string><json:string>inflammatory</json:string><json:string>cerebral</json:string><json:string>reeder</json:string><json:string>newbold</json:string><json:string>fibrin deposition</json:string><json:string>tryptophan metabolism</json:string><json:string>dendritic cells</json:string><json:string>human studies</json:string><json:string>cerebral endothelium</json:string><json:string>other receptors</json:string><json:string>vascular cell adhesion molecule</json:string><json:string>quinolinic acid</json:string><json:string>human microvascular</json:string><json:string>noncerebral malaria</json:string><json:string>parasitized erythrocytes</json:string><json:string>malaria pathogenesis</json:string><json:string>clinical disease</json:string><json:string>cytoadherence characteristics</json:string><json:string>model systems</json:string><json:string>malaria infection</json:string><json:string>endothelial receptors</json:string><json:string>human placenta</json:string><json:string>neuronal damage</json:string><json:string>pregnant women</json:string><json:string>experimental murine</json:string><json:string>plasmodium falciparum cytoadherence</json:string><json:string>cerebrospinal fluid</json:string><json:string>birth weight</json:string></teeft></keywords><author><json:item><name>STEPHEN J ROGERSON</name><affiliations><json:string>Department of Medicine (RMH), University of Melbourne, Parkville, Australia</json:string></affiliations></json:item><json:item><name>GEORGES E. GRAU</name><affiliations><json:string>Experimental Parasitology Unit, Faculty of Medicine, Université de la Méditerranée, Marseille, France</json:string></affiliations></json:item><json:item><name>NICHOLAS H. HUNT</name><affiliations><json:string>Department of Pathology, Institute for Biomedical Research, University of Sydney, Sydney, New South Wales, Australia</json:string><json:string>E-mail: nhunt@med.usyd.edu.au</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cytokines</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>endothelium</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>malaria</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>microcirculation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>placenta</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Plasmodium falciparum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>platelet</value></json:item></subject><articleId><json:string>MICC422</json:string></articleId><arkIstex>ark:/67375/WNG-6RXF8V4M-6</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of the microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>184</abstractWordCount><abstractCharCount>1325</abstractCharCount><keywordCount>7</keywordCount><score>9.208</score><pdfWordCount>10433</pdfWordCount><pdfCharCount>69308</pdfCharCount><pdfVersion>1.5</pdfVersion><pdfPageCount>18</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize></qualityIndicators><title>The Microcirculation in Severe Malaria</title><pmid><json:string>15513866</json:string></pmid><genre><json:string>review-article</json:string></genre><host><title>Microcirculation</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1549-8719</json:string></doi><issn><json:string>1073-9688</json:string></issn><eissn><json:string>1549-8719</json:string></eissn><publisherId><json:string>MICC</json:string></publisherId><volume>11</volume><issue>7</issue><pages><first>559</first><last>576</last><total>18</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2004</json:string></date><geogName></geogName><orgName><json:string>Department of Pathology</json:string><json:string>Institute for Biomedical Research, University of Sydney, Sydney, NSW</json:string><json:string>Department of Medicine</json:string><json:string>National Institutes of Health</json:string><json:string>World Health Organisation</json:string><json:string>University of Melbourne</json:string><json:string>National Health and Medical Research</json:string><json:string>Department of Pathology, Institute for Biomedical Research, University of Sydney, Sydney, New South Wales, Australia ABSTRACT Severe</json:string><json:string>RMH</json:string><json:string>Ministry of Research, Paris, France</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Taylor</json:string><json:string>In</json:string><json:string>Nicholas H. Hunt</json:string><json:string>Danny J. 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Hunt, Department of Pathology (D06), Institute for Biomedical Research, University of Sydney, Sydney, NSW 2006, Australia. E‐mail: nhunt@med.usyd.edu.au</affiliation></author><idno type="istex">5B1AF32532823B4354AF2AB842A41583B83424D1</idno><idno type="ark">ark:/67375/WNG-6RXF8V4M-6</idno><idno type="DOI">10.1080/10739680490503311</idno><idno type="unit">MICC422</idno><idno type="toTypesetVersion">file:MICC.MICC422.pdf</idno></analytic><monogr><title level="j" type="main">Microcirculation</title><title level="j" type="alt">MICROCIRCULATION</title><idno type="pISSN">1073-9688</idno><idno type="eISSN">1549-8719</idno><idno type="book-DOI">10.1111/(ISSN)1549-8719</idno><idno type="book-part-DOI">10.1111/micc.2004.11.issue-7</idno><idno type="product">MICC</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">11</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="559">559</biblScope><biblScope unit="page" to="576">576</biblScope><biblScope unit="page-count">18</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2004-10-11"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>ABSTRACT</head><p>Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. 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E‐mail: <email>nhunt@med.usyd.edu.au</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MICC.MICC422.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 7 November 2003; accepted 4 June 2004.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="188"></count><count type="linksCrossRef" number="166"></count></countGroup><titleGroup><title type="main">The Microcirculation in Severe Malaria</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>STEPHEN J</givenNames><familyName>ROGERSON</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>GEORGES E.</givenNames><familyName>GRAU</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3" corresponding="yes"><personName><givenNames>NICHOLAS H.</givenNames><familyName>HUNT</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="AU"><unparsedAffiliation>Department of Medicine (RMH), University of Melbourne, Parkville, Australia</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>Experimental Parasitology Unit, Faculty of Medicine, Université de la Méditerranée, Marseille, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="AU"><unparsedAffiliation>Department of Pathology, Institute for Biomedical Research, University of Sydney, Sydney, New South Wales, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">cytokines</keyword><keyword xml:id="k2">endothelium</keyword><keyword xml:id="k3">malaria</keyword><keyword xml:id="k4">microcirculation</keyword><keyword xml:id="k5">placenta</keyword><keyword xml:id="k6"><i>Plasmodium falciparum</i></keyword><keyword xml:id="k7">platelet</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">ABSTRACT</title><p>Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen <i>Plasmodium falciparum</i> erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of the microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>SJR is supported by the Wellcome Trust (grant 063215) and the National Health and Medical Research Council of Australia (NHMRC). GEG is supported by the PAL+ Program, French Ministry of Research, Paris, France and by WHO‐TDR, Geneva, Switzerland. NHH is supported by the NHMRC. We thank Terrie Taylor for unpublished information and for comments on the manuscript and Danny J. Milner, Jr. for <link href="#f1">Figure 1d</link>. The autopsy study cited is funded by the National Institutes of Health (grant RO1 AI34969 to Dr. Taylor).</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The Microcirculation in Severe Malaria</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The Microcirculation in Severe Malaria</title></titleInfo><name type="personal"><namePart type="given">STEPHEN J</namePart><namePart type="family">ROGERSON</namePart><affiliation>Department of Medicine (RMH), University of Melbourne, Parkville, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GEORGES E.</namePart><namePart type="family">GRAU</namePart><affiliation>Experimental Parasitology Unit, Faculty of Medicine, Université de la Méditerranée, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NICHOLAS H.</namePart><namePart type="family">HUNT</namePart><affiliation>Department of Pathology, Institute for Biomedical Research, University of Sydney, Sydney, New South Wales, Australia</affiliation><affiliation>E-mail: nhunt@med.usyd.edu.au</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2004-10-11</dateIssued><edition>Received 7 November 2003; accepted 4 June 2004.</edition><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">2</extent><extent unit="tables">3</extent><extent unit="formulas">0</extent><extent unit="references">188</extent><extent unit="linksCrossRef">166</extent></physicalDescription><abstract lang="en">Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. 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