The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension
Identifieur interne : 000299 ( Istex/Corpus ); précédent : 000298; suivant : 000300The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension
Auteurs : Nada Kherbeck ; Mathieu C. Tamby ; Guillaume Bussone ; Hanadi Dib ; Frederic Perros ; Marc Humbert ; Luc MouthonSource :
- Clinical Reviews in Allergy & Immunology [ 1080-0549 ] ; 2013-02-01.
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Abstract
Abstract: Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. In this setting, it would be important to set-up new experimental models of pulmonary arterial hypertension, in order to define novel therapeutics that specifically target immune disturbances in this devastating condition.
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DOI: 10.1007/s12016-011-8265-z
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sort="Tamby, Mathieu C" uniqKey="Tamby M" first="Mathieu C." last="Tamby">Mathieu C. Tamby</name><affiliation><mods:affiliation>Institut Cochin, INSERM U1016, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CNRS UMR 8104, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Paris Descartes, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Institut Cochin, Pavillon Gustave Roussy, 4ème étage, 8 rue Méchain, 75014, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mathieu.tamby@inserm.fr</mods:affiliation></affiliation></author><author><name sortKey="Bussone, Guillaume" sort="Bussone, Guillaume" uniqKey="Bussone G" first="Guillaume" last="Bussone">Guillaume Bussone</name><affiliation><mods:affiliation>Institut Cochin, INSERM U1016, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CNRS UMR 8104, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Paris Descartes, Paris, 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national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine-Béclère, AP-HP, Clamart, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France</mods:affiliation></affiliation></author><author><name sortKey="Humbert, Marc" sort="Humbert, Marc" uniqKey="Humbert M" first="Marc" last="Humbert">Marc Humbert</name><affiliation><mods:affiliation>Université Paris Sud, Faculté de Médecine, centre national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine-Béclère, AP-HP, Clamart, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France</mods:affiliation></affiliation></author><author><name sortKey="Mouthon, Luc" sort="Mouthon, Luc" uniqKey="Mouthon L" first="Luc" last="Mouthon">Luc Mouthon</name><affiliation><mods:affiliation>Institut Cochin, INSERM U1016, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>CNRS UMR 8104, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Paris Descartes, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical Reviews in Allergy & Immunology</title><title level="j" type="abbrev">Clinic Rev Allerg Immunol</title><idno type="ISSN">1080-0549</idno><idno type="eISSN">1559-0267</idno><imprint><publisher>Humana Press Inc</publisher><pubPlace>New York</pubPlace><date type="published" when="2013-02-01">2013-02-01</date><biblScope unit="volume">44</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="31">31</biblScope><biblScope unit="page" to="38">38</biblScope></imprint><idno type="ISSN">1080-0549</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1080-0549</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autoantibodies</term><term>Autoimmunity</term><term>Inflammation</term><term>Pulmonary arterial hypertension</term><term>Systemic sclerosis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. In this setting, it would be important to set-up new experimental models of pulmonary arterial hypertension, in order to define novel therapeutics that specifically target immune disturbances in this devastating condition.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Nada Kherbeck</name><affiliations><json:string>Institut Cochin, INSERM U1016, Paris, France</json:string><json:string>CNRS UMR 8104, Paris, France</json:string><json:string>Université Paris Descartes, Paris, France</json:string></affiliations></json:item><json:item><name>Mathieu C. Tamby</name><affiliations><json:string>Institut Cochin, INSERM U1016, Paris, France</json:string><json:string>CNRS UMR 8104, Paris, France</json:string><json:string>Université Paris Descartes, Paris, France</json:string><json:string>Institut Cochin, Pavillon Gustave Roussy, 4ème étage, 8 rue Méchain, 75014, Paris, France</json:string><json:string>E-mail: mathieu.tamby@inserm.fr</json:string></affiliations></json:item><json:item><name>Guillaume Bussone</name><affiliations><json:string>Institut Cochin, INSERM U1016, Paris, France</json:string><json:string>CNRS UMR 8104, Paris, France</json:string><json:string>Université Paris Descartes, Paris, France</json:string><json:string>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France</json:string></affiliations></json:item><json:item><name>Hanadi Dib</name><affiliations><json:string>Institut Cochin, INSERM U1016, Paris, France</json:string><json:string>CNRS UMR 8104, Paris, France</json:string><json:string>Université Paris Descartes, Paris, France</json:string></affiliations></json:item><json:item><name>Frederic Perros</name><affiliations><json:string>Université Paris Sud, Faculté de Médecine, centre national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine-Béclère, AP-HP, Clamart, France</json:string><json:string>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France</json:string></affiliations></json:item><json:item><name>Marc Humbert</name><affiliations><json:string>Université Paris Sud, Faculté de Médecine, centre national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine-Béclère, AP-HP, Clamart, France</json:string><json:string>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France</json:string></affiliations></json:item><json:item><name>Luc Mouthon</name><affiliations><json:string>Institut Cochin, INSERM U1016, Paris, France</json:string><json:string>CNRS UMR 8104, Paris, France</json:string><json:string>Université Paris Descartes, Paris, France</json:string><json:string>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Inflammation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Autoimmunity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pulmonary arterial hypertension</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Systemic sclerosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Autoantibodies</value></json:item></subject><articleId><json:string>8265</json:string><json:string>s12016-011-8265-z</json:string></articleId><arkIstex>ark:/67375/VQC-00L4TPTR-L</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>ReviewPaper</json:string></originalGenre><abstract>Abstract: Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. 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Descartes, Paris, France</affiliation><affiliation>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France</affiliation></author><idno type="istex">A7AE814F0F733849ACF9968A15589D58671779F5</idno><idno type="ark">ark:/67375/VQC-00L4TPTR-L</idno><idno type="DOI">10.1007/s12016-011-8265-z</idno><idno type="article-id">8265</idno><idno type="article-id">s12016-011-8265-z</idno></analytic><monogr><title level="j">Clinical Reviews in Allergy & Immunology</title><title level="j" type="abbrev">Clinic Rev Allerg Immunol</title><idno type="pISSN">1080-0549</idno><idno type="eISSN">1559-0267</idno><idno type="journal-ID">true</idno><idno type="issue-article-count">12</idno><idno type="volume-issue-count">3</idno><editor xml:id="book-author-0000"><persName><forename type="first">Carlo</forename><surname>Selmi</surname></persName></editor><editor xml:id="book-author-0001"><persName><forename type="first">Nancy</forename><surname>Agmon-Levin</surname></persName></editor><imprint><publisher>Humana Press Inc</publisher><pubPlace>New York</pubPlace><date type="published" when="2013-02-01"></date><biblScope unit="volume">44</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="31">31</biblScope><biblScope unit="page" to="38">38</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. In this setting, it would be important to set-up new experimental models of pulmonary arterial hypertension, in order to define novel therapeutics that specifically target immune disturbances in this devastating condition.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Inflammation</term></item><item><term>Autoimmunity</term></item><item><term>Pulmonary arterial hypertension</term></item><item><term>Systemic sclerosis</term></item><item><term>Autoantibodies</term></item></list></keywords></textClass><textClass><keywords scheme="Journal-Subject-Collection"><list><label>SC11</label><item><term>Medicine</term></item></list></keywords></textClass><textClass><keywords scheme="Journal-Subject-Group"><list><label>SCH</label><item><term>Medicine & Public Health</term></item><label>SCH11009</label><item><term>Allergology</term></item><label>SCB14000</label><item><term>Immunology</term></item><label>SCH33002</label><item><term>Internal 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OutputMedium="All"><IssueInfo IssueType="Regular" TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd><IssueTitle Language="En">Autoimmunity and the Cardiovascular System</IssueTitle><IssueArticleCount>12</IssueArticleCount><IssueHistory><OnlineDate><Year>2013</Year><Month>1</Month><Day>19</Day></OnlineDate><PrintDate><Year>2013</Year><Month>1</Month><Day>18</Day></PrintDate><CoverDate><Year>2013</Year><Month>2</Month></CoverDate><PricelistYear>2013</PricelistYear></IssueHistory><IssueCopyright><CopyrightHolderName>Springer Science+Business Media New York</CopyrightHolderName><CopyrightYear>2013</CopyrightYear></IssueCopyright></IssueInfo><IssueHeader><EditorGroup><Editor><EditorName DisplayOrder="Western"><GivenName>Carlo</GivenName><FamilyName>Selmi</FamilyName></EditorName></Editor><Editor><EditorName DisplayOrder="Western"><GivenName>Nancy</GivenName><FamilyName>Agmon-Levin</FamilyName></EditorName></Editor></EditorGroup></IssueHeader><Article ID="s12016-011-8265-z" OutputMedium="All"><ArticleInfo ArticleType="ReviewPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>8265</ArticleID><ArticleDOI>10.1007/s12016-011-8265-z</ArticleDOI><ArticleSequenceNumber>5</ArticleSequenceNumber><ArticleTitle Language="En">The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension</ArticleTitle><ArticleFirstPage>31</ArticleFirstPage><ArticleLastPage>38</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2011</Year><Month>2</Month><Day>23</Day></RegistrationDate><OnlineDate><Year>2011</Year><Month>3</Month><Day>11</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer Science+Business Media, LLC</CopyrightHolderName><CopyrightYear>2011</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1 Aff2 Aff3"><AuthorName DisplayOrder="Western"><GivenName>Nada</GivenName><FamilyName>Kherbeck</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1 Aff2 Aff3 Aff7" CorrespondingAffiliationID="Aff7"><AuthorName DisplayOrder="Western"><GivenName>Mathieu</GivenName><GivenName>C.</GivenName><FamilyName>Tamby</FamilyName></AuthorName><Contact><Phone>+33-144-412544</Phone><Fax>+33-144-412546</Fax><Email>mathieu.tamby@inserm.fr</Email></Contact></Author><Author AffiliationIDS="Aff1 Aff2 Aff3 Aff4"><AuthorName DisplayOrder="Western"><GivenName>Guillaume</GivenName><FamilyName>Bussone</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1 Aff2 Aff3"><AuthorName DisplayOrder="Western"><GivenName>Hanadi</GivenName><FamilyName>Dib</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5 Aff6"><AuthorName DisplayOrder="Western"><GivenName>Frederic</GivenName><FamilyName>Perros</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5 Aff6"><AuthorName DisplayOrder="Western"><GivenName>Marc</GivenName><FamilyName>Humbert</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1 Aff2 Aff3 Aff4"><AuthorName DisplayOrder="Western"><GivenName>Luc</GivenName><FamilyName>Mouthon</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Institut Cochin</OrgDivision><OrgName>INSERM U1016</OrgName><OrgAddress><City>Paris</City><Country Code="FR">France</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>CNRS UMR 8104</OrgName><OrgAddress><City>Paris</City><Country Code="FR">France</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgName>Université Paris Descartes</OrgName><OrgAddress><City>Paris</City><Country Code="FR">France</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique</OrgDivision><OrgName>hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP)</OrgName><OrgAddress><City>Paris</City><Country Code="FR">France</Country></OrgAddress></Affiliation><Affiliation ID="Aff5"><OrgDivision>Université Paris Sud, Faculté de Médecine, centre national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire</OrgDivision><OrgName>Hôpital Antoine-Béclère, AP-HP</OrgName><OrgAddress><City>Clamart</City><Country Code="FR">France</Country></OrgAddress></Affiliation><Affiliation ID="Aff6"><OrgName>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue</OrgName><OrgAddress><City>Le Plessis-Robinson</City><Country Code="FR">France</Country></OrgAddress></Affiliation><Affiliation ID="Aff7"><OrgName>Institut Cochin, Pavillon Gustave Roussy</OrgName><OrgAddress><Street>4ème étage, 8 rue Méchain</Street><Postcode>75014</Postcode><City>Paris</City><Country Code="FR">France</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En" OutputMedium="All"><Heading>Abstract</Heading><Para>Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. In this setting, it would be important to set-up new experimental models of pulmonary arterial hypertension, in order to define novel therapeutics that specifically target immune disturbances in this devastating condition.</Para></Abstract><KeywordGroup Language="En" OutputMedium="All"><Heading>Keywords</Heading><Keyword>Inflammation</Keyword><Keyword>Autoimmunity</Keyword><Keyword>Pulmonary arterial hypertension</Keyword><Keyword>Systemic sclerosis</Keyword><Keyword>Autoantibodies</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension</title></titleInfo><name type="personal"><namePart type="given">Nada</namePart><namePart type="family">Kherbeck</namePart><affiliation>Institut Cochin, INSERM U1016, Paris, France</affiliation><affiliation>CNRS UMR 8104, Paris, France</affiliation><affiliation>Université Paris Descartes, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Mathieu</namePart><namePart type="given">C.</namePart><namePart type="family">Tamby</namePart><affiliation>Institut Cochin, INSERM U1016, Paris, France</affiliation><affiliation>CNRS UMR 8104, Paris, France</affiliation><affiliation>Université Paris Descartes, Paris, France</affiliation><affiliation>Institut Cochin, Pavillon Gustave Roussy, 4ème étage, 8 rue Méchain, 75014, Paris, France</affiliation><affiliation>E-mail: mathieu.tamby@inserm.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guillaume</namePart><namePart type="family">Bussone</namePart><affiliation>Institut Cochin, INSERM U1016, Paris, France</affiliation><affiliation>CNRS UMR 8104, Paris, France</affiliation><affiliation>Université Paris Descartes, Paris, France</affiliation><affiliation>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hanadi</namePart><namePart type="family">Dib</namePart><affiliation>Institut Cochin, INSERM U1016, Paris, France</affiliation><affiliation>CNRS UMR 8104, Paris, France</affiliation><affiliation>Université Paris Descartes, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frederic</namePart><namePart type="family">Perros</namePart><affiliation>Université Paris Sud, Faculté de Médecine, centre national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine-Béclère, AP-HP, Clamart, France</affiliation><affiliation>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Humbert</namePart><affiliation>Université Paris Sud, Faculté de Médecine, centre national de référence de l’hypertension artérielle pulmonaire sévère, Service de Pneumologie et Réanimation Respiratoire, Hôpital Antoine-Béclère, AP-HP, Clamart, France</affiliation><affiliation>INSERM U999, Hypertension Artérielle Pulmonaire, Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luc</namePart><namePart type="family">Mouthon</namePart><affiliation>Institut Cochin, INSERM U1016, Paris, France</affiliation><affiliation>CNRS UMR 8104, Paris, France</affiliation><affiliation>Université Paris Descartes, Paris, France</affiliation><affiliation>Université Paris Descartes, Faculté de Médecine, pôle de Médecine Interne et centre de référence pour les vascularites nécrosantes et la sclérodermie systémique, hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="ReviewPaper" 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>Humana Press Inc</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2013-02-01</dateIssued><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Pulmonary arterial hypertension is characterized by a remodeling of pulmonary arteries with endothelial cell, fibroblast, and vascular smooth muscle cell activation and proliferation. Since pulmonary arterial hypertension occurs frequently in autoimmune conditions such as systemic sclerosis, inflammation and autoimmunity have been suspected to play a critical role in both idiopathic pulmonary arterial hypertension and systemic sclerosis-associated pulmonary arterial hypertension. High levels of pro-inflammatory cytokines such as interleukin-1 and interleukin-6, platelet-derived growth factor, or macrophage inflammatory protein 1 have been found in lung samples of patients with pulmonary arterial hypertension, along with inflammatory cell infiltrates mainly composed of macrophages and dendritic cells, T and B lymphocytes. In addition, circulating autoantibodies are found in the peripheral blood of patients. Thus, autoimmunity and inflammation probably play a role in the development of pulmonary arterial hypertension. In this setting, it would be important to set-up new experimental models of pulmonary arterial hypertension, in order to define novel therapeutics that specifically target immune disturbances in this devastating condition.</abstract><subject lang="en"><genre>Keywords</genre><topic>Inflammation</topic><topic>Autoimmunity</topic><topic>Pulmonary arterial hypertension</topic><topic>Systemic sclerosis</topic><topic>Autoantibodies</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Reviews in Allergy & Immunology</title></titleInfo><titleInfo type="abbreviated"><title>Clinic Rev Allerg Immunol</title></titleInfo><name type="personal"><namePart type="given">Carlo</namePart><namePart type="family">Selmi</namePart><role><roleTerm type="text">editor</roleTerm></role></name><name type="personal"><namePart type="given">Nancy</namePart><namePart type="family">Agmon-Levin</namePart><role><roleTerm type="text">editor</roleTerm></role></name><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">2013-01-19</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><subject><genre>Journal-Subject-Collection</genre><topic authority="SpringerSubjectCodes" authorityURI="SC11">Medicine</topic></subject><subject><genre>Journal-Subject-Group</genre><topic authority="SpringerSubjectCodes" authorityURI="SCH">Medicine & Public Health</topic><topic authority="SpringerSubjectCodes" authorityURI="SCH11009">Allergology</topic><topic authority="SpringerSubjectCodes" authorityURI="SCB14000">Immunology</topic><topic authority="SpringerSubjectCodes" authorityURI="SCH33002">Internal Medicine</topic></subject><identifier type="ISSN">1080-0549</identifier><identifier type="eISSN">1559-0267</identifier><identifier type="JournalID">12016</identifier><identifier type="IssueArticleCount">12</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>2013</date><detail type="issue"><title>Autoimmunity and the Cardiovascular System</title></detail><detail type="volume"><number>44</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="pages"><start>31</start><end>38</end></extent></part><recordInfo><recordOrigin>Springer Science+Business Media New York, 2013</recordOrigin></recordInfo></relatedItem><identifier type="istex">A7AE814F0F733849ACF9968A15589D58671779F5</identifier><identifier type="ark">ark:/67375/VQC-00L4TPTR-L</identifier><identifier type="DOI">10.1007/s12016-011-8265-z</identifier><identifier type="ArticleID">8265</identifier><identifier type="ArticleID">s12016-011-8265-z</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer Science+Business Media, LLC, 2011</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Springer Science+Business Media, LLC, 2011</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-00L4TPTR-L/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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