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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-17T12:06:34Z</responseDate> <request identifier=oai:HAL:hal-01560150v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-01560150v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:U917</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> <setSpec>collection:SANTE_PUB_INSERM</setSpec> <setSpec>collection:HL</setSpec> <setSpec>collection:U991</setSpec> <setSpec>collection:IRSET-CCII</setSpec> <setSpec>collection:CIC</setSpec> <setSpec>collection:CIC203</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:IRSET-1</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:NUMECAN-CIMIAD</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:NUMECAN</setSpec> <setSpec>collection:MICMAC</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>CD16-positive circulating monocytes and fibrotic manifestations of systemic sclerosis</title> <creator>Lescoat, Alain</creator> <creator>Lecureur, Valérie</creator> <creator>Roussel, Mikael</creator> <creator>Ly Sunnaram, Beatrice</creator> <creator>Ballerie, Alice</creator> <creator>Coiffier, Guillaume</creator> <creator>Jouneau, Stéphane</creator> <creator>Fardel, Olivier</creator> <creator>Fest, Thierry</creator> <creator>Jego, Patrick</creator> <contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Service d’immunologie, de thérapie cellulaire et d’hématopoïèse ; Hôpital Pontchaillou</contributor> <contributor>Microenvironnement et cancer (MiCa) ; Université de Rennes 1 (UR1) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>CHU Pontchaillou [Rennes]</contributor> <contributor>Foie, métabolismes et cancer ; Université de Rennes 1 (UR1) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Centre d'Investigation Clinique [Rennes] (CIC) ; Université de Rennes 1 (UR1) - Hôpital Pontchaillou - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor> <description>International audience</description> <source>ISSN: 0770-3198</source> <source>EISSN: 1434-9949</source> <source>Clinical Rheumatology</source> <publisher>Springer Verlag</publisher> <identifier>hal-01560150</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01560150</identifier> <source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01560150</source> <source>Clinical Rheumatology, Springer Verlag, 2017, 36 (7), pp.1649--1654. 〈10.1007/s10067-017-3597-6〉</source> <identifier>DOI : 10.1007/s10067-017-3597-6</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1007/s10067-017-3597-6</relation> <identifier>PUBMED : 28293753</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/28293753</relation> <language>en</language> <subject lang=en>cd16</subject> <subject lang=en> interstitial lung disease</subject> <subject lang=en> monocytes</subject> <subject lang=en> pulmonary arterial hypertension</subject> <subject lang=en> systemic sclerosis</subject> <subject>[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>The objective of this study is to assess the association of clinical manifestations of systemic sclerosis (SSc) with the absolute count of circulating blood monocyte subpopulations according to their membrane expression of CD16. Forty-eight consecutive patients fulfilling the 2013 ACR/EULAR classification criteria for SSc were included in this cross-sectional study. CD16+ monocyte absolute count was defined by flow cytometry and confronted to the clinical characteristics of SSc patients. Twenty-three healthy donors (HD) were randomly selected for comparison. SSc patients had an increased number of total circulating blood monocytes compared to HD (p < 0.001). The CD16- subpopulation absolute count was increased in SSc patients compared to HD (p < 0.001) but was similar in limited SSc (lSSc) and diffuse SSc (dSSc). On the contrary, the CD16+ population absolute count was increased in dSSc compared to both HD and lSSc patients (dSSc 0.071 Giga/L (+/- 0.034) vs HD 0.039 Giga/L (+/- 0.030), p < 0.01, and dSSc 0.071 Giga/L (+/- 0.034) vs lSSc 0.048 Giga/L (+/- 0.024), p < 0.05). The CD16+ monocyte subpopulation absolute count was significantly correlated with the severity of skin fibrosis evaluated by the modified Rodnan skin score (p < 0.001). The CD16+ monocyte subpopulation was also associated with pulmonary fibrosis (p < 0.05), with the severity of the restrictive ventilatory defect evaluated by total lung capacity (p < 0.05) and with the pulmonary function impairment reflected by diffusing capacity of the lungs for carbon monoxyde measures (p < 0.01). These results suggest that CD16+ monocytes are associated with the main fibrotic manifestations of SSc and their role in the pathogenesis of fibrosis in this autoimmune disorder should therefore be further considered.</description> <date>2017</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>