A novel mechanism for immune regulation after human lung transplantation
Identifieur interne : 000941 ( Pmc/Curation ); précédent : 000940; suivant : 000942A novel mechanism for immune regulation after human lung transplantation
Auteurs : Thalachallour Mohanakumar ; Monal Sharma ; Sandhya Bansal ; Ranjithkumar Ravichandran ; Michael A. Smith ; Ross M. BremnerSource :
- The Journal of Thoracic and Cardiovascular Surgery [ 0022-5223 ] ; 2019.
Abstract
Lung transplantation is therapeutic for end-stage lung disease, but survival is limited due to bronchiolitis obliterans syndrome and restrictive chronic lung allograft dysfunction. We sought a common denominator in lung transplant recipients, analyzing risk factors that trigger immune responses that lead to bronchiolitis obliterans syndrome.
We collected blood from patients who underwent lung transplant at our institution. Exosomes were isolated from the sera of recipients with risk factors for chronic rejection and from stable recipients. Exosomes were analyzed with western blot, using antibodies to lung self-antigens K alpha 1 tubulin and collagen-V, costimulatory molecules (costimulatory molecule 80, costimulatory molecule 86), transcription factors (nuclear factor kappa-light-chain-enhancer of activated B cells, hypoxia-inducible factor 1α, Class II Major Histocompatibility Complex Transactivator), and 20S proteasome.
Of the 90 patients included, we identified 5 with grade 3 primary graft dysfunction, 5 without, 15 with respiratory viral infection, 10 with acute rejection, 10 with donor-specific antibodies (DSA), 5 without DSA, and 10 who were stable for exosome isolation. Recipients with grade 3 primary graft dysfunction, respiratory viral infection, acute rejection, and DSA had exosomes containing self-antigens; exosomes from stable recipients did not. Exosomes from recipients with grade 3 primary graft dysfunction, acute rejection, and DSA also demonstrated costimulatory molecule 80, costimulatory molecule 86, major histocompatibility complex class II, transcription factor, and 20S proteasome.
Transplanted lungs with grade 3 primary graft dysfunction, symptomatic respiratory viral infection, acute rejection, and immune responses induce exosomes that contain self-antigens, costimulatory molecules, major histocompatibility complex class II, transcription factors, and 20S proteasome. Release of circulating exosomes post-transplant from the aforementioned stress-inducing insults augment immunity and may play an important role in the pathogenesis of bronchiolitis obliterans syndrome.
Url:
DOI: 10.1016/j.jtcvs.2018.12.105
PubMed: 31288367
PubMed Central: 6625531
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A novel mechanism for immune regulation after human lung transplantation</title><author><name sortKey="Mohanakumar, Thalachallour" sort="Mohanakumar, Thalachallour" uniqKey="Mohanakumar T" first="Thalachallour" last="Mohanakumar">Thalachallour Mohanakumar</name></author><author><name sortKey="Sharma, Monal" sort="Sharma, Monal" uniqKey="Sharma M" first="Monal" last="Sharma">Monal Sharma</name></author><author><name sortKey="Bansal, Sandhya" sort="Bansal, Sandhya" uniqKey="Bansal S" first="Sandhya" last="Bansal">Sandhya Bansal</name></author><author><name sortKey="Ravichandran, Ranjithkumar" sort="Ravichandran, Ranjithkumar" uniqKey="Ravichandran R" first="Ranjithkumar" last="Ravichandran">Ranjithkumar Ravichandran</name></author><author><name sortKey="Smith, Michael A" sort="Smith, Michael A" uniqKey="Smith M" first="Michael A." last="Smith">Michael A. Smith</name></author><author><name sortKey="Bremner, Ross M" sort="Bremner, Ross M" uniqKey="Bremner R" first="Ross M." last="Bremner">Ross M. Bremner</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31288367</idno><idno type="pmc">6625531</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625531</idno><idno type="RBID">PMC:6625531</idno><idno type="doi">10.1016/j.jtcvs.2018.12.105</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000941</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000941</idno><idno type="wicri:Area/Pmc/Curation">000941</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000941</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">A novel mechanism for immune regulation after human lung transplantation</title><author><name sortKey="Mohanakumar, Thalachallour" sort="Mohanakumar, Thalachallour" uniqKey="Mohanakumar T" first="Thalachallour" last="Mohanakumar">Thalachallour Mohanakumar</name></author><author><name sortKey="Sharma, Monal" sort="Sharma, Monal" uniqKey="Sharma M" first="Monal" last="Sharma">Monal Sharma</name></author><author><name sortKey="Bansal, Sandhya" sort="Bansal, Sandhya" uniqKey="Bansal S" first="Sandhya" last="Bansal">Sandhya Bansal</name></author><author><name sortKey="Ravichandran, Ranjithkumar" sort="Ravichandran, Ranjithkumar" uniqKey="Ravichandran R" first="Ranjithkumar" last="Ravichandran">Ranjithkumar Ravichandran</name></author><author><name sortKey="Smith, Michael A" sort="Smith, Michael A" uniqKey="Smith M" first="Michael A." last="Smith">Michael A. Smith</name></author><author><name sortKey="Bremner, Ross M" sort="Bremner, Ross M" uniqKey="Bremner R" first="Ross M." last="Bremner">Ross M. Bremner</name></author></analytic><series><title level="j">The Journal of Thoracic and Cardiovascular Surgery</title><idno type="ISSN">0022-5223</idno><idno type="eISSN">1097-685X</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>Objective</title><p>Lung transplantation is therapeutic for end-stage lung disease, but survival is limited due to bronchiolitis obliterans syndrome and restrictive chronic lung allograft dysfunction. We sought a common denominator in lung transplant recipients, analyzing risk factors that trigger immune responses that lead to bronchiolitis obliterans syndrome.</p></sec><sec><title>Methods</title><p>We collected blood from patients who underwent lung transplant at our institution. Exosomes were isolated from the sera of recipients with risk factors for chronic rejection and from stable recipients. Exosomes were analyzed with western blot, using antibodies to lung self-antigens K alpha 1 tubulin and collagen-V, costimulatory molecules (costimulatory molecule 80, costimulatory molecule 86), transcription factors (nuclear factor kappa-light-chain-enhancer of activated B cells, hypoxia-inducible factor 1α, Class II Major Histocompatibility Complex Transactivator), and 20S proteasome.</p></sec><sec><title>Results</title><p>Of the 90 patients included, we identified 5 with grade 3 primary graft dysfunction, 5 without, 15 with respiratory viral infection, 10 with acute rejection, 10 with donor-specific antibodies (DSA), 5 without DSA, and 10 who were stable for exosome isolation. Recipients with grade 3 primary graft dysfunction, respiratory viral infection, acute rejection, and DSA had exosomes containing self-antigens; exosomes from stable recipients did not. Exosomes from recipients with grade 3 primary graft dysfunction, acute rejection, and DSA also demonstrated costimulatory molecule 80, costimulatory molecule 86, major histocompatibility complex class II, transcription factor, and 20S proteasome.</p></sec><sec><title>Conclusions</title><p>Transplanted lungs with grade 3 primary graft dysfunction, symptomatic respiratory viral infection, acute rejection, and immune responses induce exosomes that contain self-antigens, costimulatory molecules, major histocompatibility complex class II, transcription factors, and 20S proteasome. Release of circulating exosomes post-transplant from the aforementioned stress-inducing insults augment immunity and may play an important role in the pathogenesis of bronchiolitis obliterans syndrome.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Arcasoy, S M" uniqKey="Arcasoy S">S.M. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Thorac Cardiovasc Surg</journal-id><journal-id journal-id-type="iso-abbrev">J. Thorac. Cardiovasc. Surg</journal-id><journal-title-group><journal-title>The Journal of Thoracic and Cardiovascular Surgery</journal-title></journal-title-group><issn pub-type="ppub">0022-5223</issn><issn pub-type="epub">1097-685X</issn><publisher><publisher-name>Mosby</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31288367</article-id><article-id pub-id-type="pmc">6625531</article-id><article-id pub-id-type="publisher-id">S0022-5223(19)30343-5</article-id><article-id pub-id-type="doi">10.1016/j.jtcvs.2018.12.105</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>A novel mechanism for immune regulation after human lung transplantation</article-title></title-group><contrib-group><contrib contrib-type="author" id="au1"><name><surname>Mohanakumar</surname><given-names>Thalachallour</given-names></name><degrees>PhD</degrees><email>Tm.kumar@dignityhealth.org</email><xref rid="cor1" ref-type="corresp">∗</xref></contrib><contrib contrib-type="author" id="au2"><name><surname>Sharma</surname><given-names>Monal</given-names></name><degrees>PhD</degrees></contrib><contrib contrib-type="author" id="au3"><name><surname>Bansal</surname><given-names>Sandhya</given-names></name><degrees>PhD</degrees></contrib><contrib contrib-type="author" id="au4"><name><surname>Ravichandran</surname><given-names>Ranjithkumar</given-names></name><degrees>PhD</degrees></contrib><contrib contrib-type="author" id="au5"><name><surname>Smith</surname><given-names>Michael A.</given-names></name><degrees>MD</degrees></contrib><contrib contrib-type="author" id="au6"><name><surname>Bremner</surname><given-names>Ross M.</given-names></name><degrees>MD, PhD</degrees></contrib></contrib-group><aff id="aff1">Norton Thoracic Institute, St Joseph's Hospital and Medical Center, Phoenix, Ariz</aff><author-notes><corresp id="cor1"><label>∗</label>Address for reprints: Thalachallour Mohanakumar, PhD, Norton Thoracic Institute, St Joseph's Hospital and Medical Center, 124 W Thomas Rd, Suite 105, Phoenix, AZ 85013. <email>Tm.kumar@dignityhealth.org</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>12</day><month>2</month><year>2019</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>5</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>12</day><month>2</month><year>2019</year></pub-date><volume>157</volume><issue>5</issue><fpage>2096</fpage><lpage>2106</lpage><history><date date-type="received"><day>22</day><month>6</month><year>2018</year></date><date date-type="rev-recd"><day>13</day><month>11</month><year>2018</year></date><date date-type="accepted"><day>2</day><month>12</month><year>2018</year></date></history><permissions><copyright-statement>© 2019 by The American Association for Thoracic Surgery.</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>The American Association for Thoracic Surgery</copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="abs0010"><sec><title>Objective</title><p>Lung transplantation is therapeutic for end-stage lung disease, but survival is limited due to bronchiolitis obliterans syndrome and restrictive chronic lung allograft dysfunction. We sought a common denominator in lung transplant recipients, analyzing risk factors that trigger immune responses that lead to bronchiolitis obliterans syndrome.</p></sec><sec><title>Methods</title><p>We collected blood from patients who underwent lung transplant at our institution. Exosomes were isolated from the sera of recipients with risk factors for chronic rejection and from stable recipients. Exosomes were analyzed with western blot, using antibodies to lung self-antigens K alpha 1 tubulin and collagen-V, costimulatory molecules (costimulatory molecule 80, costimulatory molecule 86), transcription factors (nuclear factor kappa-light-chain-enhancer of activated B cells, hypoxia-inducible factor 1α, Class II Major Histocompatibility Complex Transactivator), and 20S proteasome.</p></sec><sec><title>Results</title><p>Of the 90 patients included, we identified 5 with grade 3 primary graft dysfunction, 5 without, 15 with respiratory viral infection, 10 with acute rejection, 10 with donor-specific antibodies (DSA), 5 without DSA, and 10 who were stable for exosome isolation. Recipients with grade 3 primary graft dysfunction, respiratory viral infection, acute rejection, and DSA had exosomes containing self-antigens; exosomes from stable recipients did not. Exosomes from recipients with grade 3 primary graft dysfunction, acute rejection, and DSA also demonstrated costimulatory molecule 80, costimulatory molecule 86, major histocompatibility complex class II, transcription factor, and 20S proteasome.</p></sec><sec><title>Conclusions</title><p>Transplanted lungs with grade 3 primary graft dysfunction, symptomatic respiratory viral infection, acute rejection, and immune responses induce exosomes that contain self-antigens, costimulatory molecules, major histocompatibility complex class II, transcription factors, and 20S proteasome. Release of circulating exosomes post-transplant from the aforementioned stress-inducing insults augment immunity and may play an important role in the pathogenesis of bronchiolitis obliterans syndrome.</p></sec></abstract><kwd-group id="kwrds0010"><title>Key Words</title><kwd>lung transplant</kwd><kwd>circulatory exosomes</kwd><kwd>rejection</kwd><kwd>primary graft dysfunction</kwd><kwd>novel mechanism</kwd><kwd>acute rejection</kwd><kwd>DSA</kwd></kwd-group><kwd-group id="kwrds0015"><title>Abbreviations and Acronyms</title><kwd>Abs, antibodies</kwd><kwd>AEC, airway epithelial cell line</kwd><kwd>AR, acute rejection</kwd><kwd>BALF, bronchoalveolar lavage fluid</kwd><kwd>BOS, bronchiolitis obliterans syndrome</kwd><kwd>CD80, costimulatory molecule 80</kwd><kwd>CD86, costimulatory molecule 86</kwd><kwd>CIITA, Class II Major Histocompatibility Complex Transactivator</kwd><kwd>CLAD, chronic lung allograft dysfunction</kwd><kwd>Col-V, collagen V</kwd><kwd>CR, chronic rejection</kwd><kwd>DSA, donor-specific antibodies</kwd><kwd>HIF-1α, hypoxia-inducible factor 1α</kwd><kwd>HLA, human leukocyte antigen</kwd><kwd>ICAM, intercellular adhesion molecule</kwd><kwd>Kα1T, K alpha 1 tubulin</kwd><kwd>LTx, lung transplantation</kwd><kwd>LTxRs, lung transplant recipients</kwd><kwd>MHC, major histocompatibility complex</kwd><kwd>miRNA, microRNA</kwd><kwd>NF-κβ, nuclear factor kappa-light-chain-enhancer of activated B cells</kwd><kwd>PBS, phosphate-buffered saline</kwd><kwd>PGD, primary graft dysfunction</kwd><kwd>RVI, respiratory viral infection</kwd><kwd>SAgs, self-antigens</kwd><kwd>VCAM, vascular cell adhesion molecule</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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