CFTR regulates B cell activation and lymphoid follicle development
Identifieur interne : 000983 ( Main/Exploration ); précédent : 000982; suivant : 000984CFTR regulates B cell activation and lymphoid follicle development
Auteurs : Francesca Polverino [États-Unis] ; Bao Lu [États-Unis] ; Joselyn Rojas Quintero [États-Unis] ; Sara O. Vargas [États-Unis] ; Avignat S. Patel [États-Unis] ; Caroline A. Owen [États-Unis] ; Norma P. Gerard [États-Unis] ; Craig Gerard [États-Unis] ; Manuela Cernadas [États-Unis]Source :
- Respiratory Research [ 1465-9921 ] ; 2019.
Abstract
Cystic fibrosis (CF) is an inherited disorder caused by mutations in the CF transmembrane conductance regulator (CFTR) gene that promotes persistent lung infection and inflammation and progressive loss of lung function. Patients with CF have increased lung lymphoid follicles (LFs) and B cell-activating factor of tumor necrosis factor family (BAFF) that regulates B cell survival and maturation. A direct role for CFTR in B cell activation and disease pathogenesis in CF remains unclear.
The number of LFs, BAFF+, TLR4+ and proliferation marker Ki67+ B cells in lung explants or resections from subjects with CF and normal controls was quantified by immunostaining. The role of CFTR in B cell activation and LF development was then examined in two independent cohorts of uninfected CFTR-deficient mice (
There was a significant increase in well-formed LFs in subjects with CF compared to normal controls. Increased B cell activation and proliferation was observed in lung LFs from CF subjects as was quantified by a significant increase in B cell BAFF, TLR4 and Ki67 expression. Uninfected
These data support a direct role for CFTR in B cell activation, proliferation and inflammatory cytokine production that promotes lung LF follicle development in cystic fibrosis.
Url:
DOI: 10.1186/s12931-019-1103-1
PubMed: 31262295
PubMed Central: 6604167
Affiliations:
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first="Francesca" last="Polverino">Francesca Polverino</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2168 186X</institution-id><institution-id institution-id-type="GRID">grid.134563.6</institution-id><institution>Asthma and Airway Disease Research Center,</institution><institution>University of Arizona,</institution></institution-wrap>Tucson, AZ 85718 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Tucson</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0367 7826</institution-id><institution-id institution-id-type="GRID">grid.280401.f</institution-id><institution>Lovelace Respiratory Research Institute,</institution></institution-wrap>Albuquerque, NM 87108 USA</nlm:aff><country 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Gerard</name><affiliation wicri:level="2"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0378 8438</institution-id><institution-id institution-id-type="GRID">grid.2515.3</institution-id><institution>Division of Respiratory Diseases, Department of Medicine,</institution><institution>Boston Children’s Hospital,</institution></institution-wrap>Boston, MA 02115 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Boston</wicri:cityArea></affiliation></author><author><name sortKey="Gerard, Craig" sort="Gerard, Craig" uniqKey="Gerard C" first="Craig" last="Gerard">Craig Gerard</name><affiliation wicri:level="2"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0378 8438</institution-id><institution-id institution-id-type="GRID">grid.2515.3</institution-id><institution>Division of Respiratory Diseases, Department of Medicine,</institution><institution>Boston Children’s Hospital,</institution></institution-wrap>Boston, MA 02115 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Boston</wicri:cityArea></affiliation></author><author><name sortKey="Cernadas, Manuela" sort="Cernadas, Manuela" uniqKey="Cernadas M" first="Manuela" last="Cernadas">Manuela Cernadas</name><affiliation wicri:level="2"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0378 8438</institution-id><institution-id institution-id-type="GRID">grid.2515.3</institution-id><institution>Division of Respiratory Diseases, Department of Medicine,</institution><institution>Boston Children’s Hospital,</institution></institution-wrap>Boston, MA 02115 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Boston</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff7">Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston</wicri:cityArea></affiliation></author></analytic><series><title level="j">Respiratory Research</title><idno type="ISSN">1465-9921</idno><idno type="eISSN">1465-993X</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p id="Par1">Cystic fibrosis (CF) is an inherited disorder caused by mutations in the CF transmembrane conductance regulator (CFTR) gene that promotes persistent lung infection and inflammation and progressive loss of lung function. Patients with CF have increased lung lymphoid follicles (LFs) and B cell-activating factor of tumor necrosis factor family (BAFF) that regulates B cell survival and maturation. A direct role for CFTR in B cell activation and disease pathogenesis in CF remains unclear.</p></sec><sec><title>Methods</title><p id="Par2">The number of LFs, BAFF<sup>+</sup>, TLR4<sup>+</sup> and proliferation marker Ki67<sup>+</sup> B cells in lung explants or resections from subjects with CF and normal controls was quantified by immunostaining. The role of CFTR in B cell activation and LF development was then examined in two independent cohorts of uninfected CFTR-deficient mice (<italic>Cftr</italic><sup><italic>−/−</italic></sup>) and wild type controls. The number of lung LFs, B cells and BAFF<sup>+</sup>, CXCR4<sup>+</sup>, immunoglobulin G<sup>+</sup> B cells was examined by immunostaining. Lung and splenocyte B cell activation marker and major histocompatibility complex class II (MHC class II) expression was quantified by flow cytometry. Inflammatory cytokine levels were measured in supernatants from isolated B cells from <italic>Cftr</italic><sup><italic>−/−</italic></sup> and wild type mice stimulated in vitro with <italic>Pseudomonas aeruginosa</italic> lipopolysaccharide (LPS).</p></sec><sec><title>Results</title><p id="Par3">There was a significant increase in well-formed LFs in subjects with CF compared to normal controls. Increased B cell activation and proliferation was observed in lung LFs from CF subjects as was quantified by a significant increase in B cell BAFF, TLR4 and Ki67 expression. Uninfected <italic>Cftr</italic><sup><italic>−/−</italic></sup> mice had increased lung LFs and BAFF<sup>+</sup> and CXCR4<sup>+</sup> B cells compared to wild type controls. Lung B cells isolated from uninfected <italic>Cftr</italic><sup><italic>−/−</italic></sup> mice demonstrated increased MHC class II expression. In vitro, isolated B cells from <italic>Cftr</italic><sup><italic>−/−</italic></sup> mice produced increased IL-6 when stimulated with LPS compared to wild type controls.</p></sec><sec><title>Conclusions</title><p id="Par4">These data support a direct role for CFTR in B cell activation, proliferation and inflammatory cytokine production that promotes lung LF follicle development in cystic fibrosis.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Montoro, Dt" uniqKey="Montoro D">DT Montoro</name></author><author><name sortKey="Haber, Al" uniqKey="Haber A">AL Haber</name></author><author><name sortKey="Biton, M" uniqKey="Biton M">M Biton</name></author><author><name sortKey="Vinarsky, V" uniqKey="Vinarsky V">V Vinarsky</name></author><author><name sortKey="Lin, B" uniqKey="Lin B">B Lin</name></author><author><name sortKey="Birket, Se" uniqKey="Birket S">SE Birket</name></author><author><name 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Craig" sort="Gerard, Craig" uniqKey="Gerard C" first="Craig" last="Gerard">Craig Gerard</name><name sortKey="Gerard, Norma P" sort="Gerard, Norma P" uniqKey="Gerard N" first="Norma P." last="Gerard">Norma P. Gerard</name><name sortKey="Lu, Bao" sort="Lu, Bao" uniqKey="Lu B" first="Bao" last="Lu">Bao Lu</name><name sortKey="Owen, Caroline A" sort="Owen, Caroline A" uniqKey="Owen C" first="Caroline A." last="Owen">Caroline A. Owen</name><name sortKey="Owen, Caroline A" sort="Owen, Caroline A" uniqKey="Owen C" first="Caroline A." last="Owen">Caroline A. Owen</name><name sortKey="Patel, Avignat S" sort="Patel, Avignat S" uniqKey="Patel A" first="Avignat S." last="Patel">Avignat S. Patel</name><name sortKey="Polverino, Francesca" sort="Polverino, Francesca" uniqKey="Polverino F" first="Francesca" last="Polverino">Francesca Polverino</name><name sortKey="Quintero, Joselyn Rojas" sort="Quintero, Joselyn Rojas" uniqKey="Quintero J" first="Joselyn Rojas" last="Quintero">Joselyn Rojas Quintero</name><name sortKey="Vargas, Sara O" sort="Vargas, Sara O" uniqKey="Vargas S" first="Sara O." last="Vargas">Sara O. Vargas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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