The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension
Identifieur interne : 003A43 ( Main/Exploration ); précédent : 003A42; suivant : 003A44The Role of Inflammation and Autoimmunity in the Pathophysiology of Pulmonary Arterial Hypertension
Auteurs : Nada Kherbeck [France] ; Mathieu C. Tamby [France] ; Guillaume Bussone [France] ; Hanadi Dib [France] ; Frederic Perros [France] ; Marc Humbert [France] ; Luc Mouthon [France]Source :
- 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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type="university">Université Paris-Descartes</orgName></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><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Orsay</li><li>Paris</li></settlement><orgName><li>Université Paris-Descartes</li><li>Université Paris-Sud</li></orgName></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Kherbeck, Nada" sort="Kherbeck, Nada" uniqKey="Kherbeck N" first="Nada" last="Kherbeck">Nada Kherbeck</name></region><name sortKey="Bussone, Guillaume" sort="Bussone, Guillaume" uniqKey="Bussone G" first="Guillaume" last="Bussone">Guillaume Bussone</name><name sortKey="Bussone, Guillaume" sort="Bussone, Guillaume" uniqKey="Bussone G" first="Guillaume" last="Bussone">Guillaume Bussone</name><name sortKey="Bussone, Guillaume" sort="Bussone, Guillaume" uniqKey="Bussone G" first="Guillaume" last="Bussone">Guillaume Bussone</name><name sortKey="Bussone, Guillaume" sort="Bussone, Guillaume" uniqKey="Bussone G" first="Guillaume" last="Bussone">Guillaume Bussone</name><name sortKey="Dib, Hanadi" sort="Dib, Hanadi" uniqKey="Dib H" first="Hanadi" last="Dib">Hanadi Dib</name><name sortKey="Dib, Hanadi" sort="Dib, Hanadi" uniqKey="Dib H" first="Hanadi" last="Dib">Hanadi Dib</name><name sortKey="Dib, Hanadi" sort="Dib, Hanadi" uniqKey="Dib H" first="Hanadi" last="Dib">Hanadi Dib</name><name sortKey="Humbert, Marc" sort="Humbert, Marc" uniqKey="Humbert M" first="Marc" last="Humbert">Marc Humbert</name><name sortKey="Humbert, Marc" sort="Humbert, Marc" uniqKey="Humbert M" first="Marc" last="Humbert">Marc Humbert</name><name sortKey="Kherbeck, Nada" sort="Kherbeck, Nada" uniqKey="Kherbeck N" first="Nada" last="Kherbeck">Nada Kherbeck</name><name sortKey="Kherbeck, Nada" sort="Kherbeck, Nada" uniqKey="Kherbeck N" first="Nada" last="Kherbeck">Nada Kherbeck</name><name sortKey="Mouthon, Luc" sort="Mouthon, Luc" uniqKey="Mouthon L" first="Luc" last="Mouthon">Luc Mouthon</name><name sortKey="Mouthon, Luc" sort="Mouthon, Luc" uniqKey="Mouthon L" first="Luc" last="Mouthon">Luc Mouthon</name><name sortKey="Mouthon, Luc" sort="Mouthon, Luc" uniqKey="Mouthon L" first="Luc" last="Mouthon">Luc Mouthon</name><name sortKey="Mouthon, Luc" sort="Mouthon, Luc" uniqKey="Mouthon L" first="Luc" last="Mouthon">Luc Mouthon</name><name sortKey="Perros, Frederic" sort="Perros, Frederic" uniqKey="Perros F" first="Frederic" last="Perros">Frederic Perros</name><name sortKey="Perros, Frederic" sort="Perros, Frederic" uniqKey="Perros F" first="Frederic" last="Perros">Frederic Perros</name><name sortKey="Tamby, Mathieu C" sort="Tamby, Mathieu C" uniqKey="Tamby M" first="Mathieu C." last="Tamby">Mathieu C. Tamby</name><name sortKey="Tamby, Mathieu C" sort="Tamby, Mathieu C" uniqKey="Tamby M" first="Mathieu C." last="Tamby">Mathieu C. Tamby</name><name sortKey="Tamby, Mathieu C" sort="Tamby, Mathieu C" uniqKey="Tamby M" first="Mathieu C." last="Tamby">Mathieu C. Tamby</name><name sortKey="Tamby, Mathieu C" sort="Tamby, Mathieu C" uniqKey="Tamby M" first="Mathieu C." last="Tamby">Mathieu C. Tamby</name><name sortKey="Tamby, Mathieu C" sort="Tamby, Mathieu C" uniqKey="Tamby M" first="Mathieu C." last="Tamby">Mathieu C. Tamby</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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