Very Late Antigen (VLA)-1 Blockade Markedly Promotes Survival of Corneal Allografts
Identifieur interne : 002761 ( Ncbi/Merge ); précédent : 002760; suivant : 002762Very Late Antigen (VLA)-1 Blockade Markedly Promotes Survival of Corneal Allografts
Auteurs : Lu Chen [États-Unis] ; Syed Huq [États-Unis] ; Humphrey Gardner [États-Unis] ; Antonin R. De Fougerolles [États-Unis] ; Stefano Barabino [États-Unis] ; M. Reza Dana [États-Unis]Source :
- Archives of ophthalmology [ 0003-9950 ] ; 2007.
Abstract
To investigate the role of very late antigen 1 (VLA-1) (also known as integrin receptor
Cell infiltration and vasculogenesis (both angiogenesis and lymphangiogenesis) associated with allodisparate corneal transplantation were assessed in VLA-1—deficient conditions and controls by immunofluorescent microscopic studies. Corneal allograft survival was also assessed after anti—VLA-1 antibody treatment and in VLA-1 knockout recipient mice.
Anti—VLA-1 antibody treatment leads to a profound reduction in the granulocytic, monocytic, and T-cell infiltration after corneal transplantation. In addition, corneal angiogenesis and lymphangiogenesis were both significantly suppressed in VLA-1 knockout mice. Remarkably, universal graft survival was observed in both anti—VLA-1 antibody treatment and knockout mice.
Very late antigen 1 blockade markedly reduces inflammation and inflammation-induced tissue responses, including vasculogenic responses, associated with corneal transplantation and promotes allograft survival.
These studies offer insights into important integrin-mediated mechanisms of corneal transplant—related inflammation and provide possible new integrin-based immunotherapies for transplant rejection.
Url:
DOI: 10.1001/archopht.125.6.783
PubMed: 17562989
PubMed Central: 2677688
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<author><name sortKey="Dana, M Reza" sort="Dana, M Reza" uniqKey="Dana M" first="M. Reza" last="Dana">M. Reza Dana</name>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objective</title>
<p id="P1">To investigate the role of very late antigen 1 (VLA-1) (also known as integrin receptor <italic>α</italic>
<sub>1</sub>
β<sub>1</sub>
) in corneal transplantation inflammation and allograft survival.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">Cell infiltration and vasculogenesis (both angiogenesis and lymphangiogenesis) associated with allodisparate corneal transplantation were assessed in VLA-1—deficient conditions and controls by immunofluorescent microscopic studies. Corneal allograft survival was also assessed after anti—VLA-1 antibody treatment and in VLA-1 knockout recipient mice.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">Anti—VLA-1 antibody treatment leads to a profound reduction in the granulocytic, monocytic, and T-cell infiltration after corneal transplantation. In addition, corneal angiogenesis and lymphangiogenesis were both significantly suppressed in VLA-1 knockout mice. Remarkably, universal graft survival was observed in both anti—VLA-1 antibody treatment and knockout mice.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">Very late antigen 1 blockade markedly reduces inflammation and inflammation-induced tissue responses, including vasculogenic responses, associated with corneal transplantation and promotes allograft survival.</p>
</sec>
<sec id="S5"><title>Clinical Relevance</title>
<p id="P5">These studies offer insights into important integrin-mediated mechanisms of corneal transplant—related inflammation and provide possible new integrin-based immunotherapies for transplant rejection.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">7706534</journal-id>
<journal-id journal-id-type="pubmed-jr-id">808</journal-id>
<journal-id journal-id-type="nlm-ta">Arch Ophthalmol</journal-id>
<journal-title>Archives of ophthalmology</journal-title>
<issn pub-type="ppub">0003-9950</issn>
<issn pub-type="epub">1538-3601</issn>
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<article-id pub-id-type="pmc">2677688</article-id>
<article-id pub-id-type="doi">10.1001/archopht.125.6.783</article-id>
<article-id pub-id-type="manuscript">NIHMS24670</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Very Late Antigen (VLA)-1 Blockade Markedly Promotes Survival of Corneal Allografts</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Lu</given-names>
</name>
<degrees>MD, PhD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
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<contrib contrib-type="author"><name><surname>Huq</surname>
<given-names>Syed</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Gardner</surname>
<given-names>Humphrey</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>de Fougerolles</surname>
<given-names>Antonin R.</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Barabino</surname>
<given-names>Stefano</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dana</surname>
<given-names>M. Reza</given-names>
</name>
<degrees>MD, MSc, MPH</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Laboratory of Immunology, Schepens Eye Research Institute and Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA</aff>
<aff id="A2"><label>2</label>
Research Pathology, Biogen Idec, Cambridge, MA</aff>
<author-notes><corresp id="CR1">Corresponding & reprint request contact author: Dr. Dana, Schepens Eye Research Institute, Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA; Phone: 617-912-7404; Fax: 617-912-0117; email: <email>dana@vision.eri.harvard.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>2</day>
<month>4</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="ppub"><month>6</month>
<year>2007</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>6</day>
<month>5</month>
<year>2009</year>
</pub-date>
<volume>125</volume>
<issue>6</issue>
<fpage>783</fpage>
<lpage>788</lpage>
<abstract><sec id="S1"><title>Objective</title>
<p id="P1">To investigate the role of very late antigen 1 (VLA-1) (also known as integrin receptor <italic>α</italic>
<sub>1</sub>
β<sub>1</sub>
) in corneal transplantation inflammation and allograft survival.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">Cell infiltration and vasculogenesis (both angiogenesis and lymphangiogenesis) associated with allodisparate corneal transplantation were assessed in VLA-1—deficient conditions and controls by immunofluorescent microscopic studies. Corneal allograft survival was also assessed after anti—VLA-1 antibody treatment and in VLA-1 knockout recipient mice.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">Anti—VLA-1 antibody treatment leads to a profound reduction in the granulocytic, monocytic, and T-cell infiltration after corneal transplantation. In addition, corneal angiogenesis and lymphangiogenesis were both significantly suppressed in VLA-1 knockout mice. Remarkably, universal graft survival was observed in both anti—VLA-1 antibody treatment and knockout mice.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">Very late antigen 1 blockade markedly reduces inflammation and inflammation-induced tissue responses, including vasculogenic responses, associated with corneal transplantation and promotes allograft survival.</p>
</sec>
<sec id="S5"><title>Clinical Relevance</title>
<p id="P5">These studies offer insights into important integrin-mediated mechanisms of corneal transplant—related inflammation and provide possible new integrin-based immunotherapies for transplant rejection.</p>
</sec>
</abstract>
<contract-num rid="EY1">R01 EY012963-07</contract-num>
<contract-sponsor id="EY1">National Eye Institute : NEI</contract-sponsor>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Massachusetts</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Chen, Lu" sort="Chen, Lu" uniqKey="Chen L" first="Lu" last="Chen">Lu Chen</name>
</region>
<name sortKey="Barabino, Stefano" sort="Barabino, Stefano" uniqKey="Barabino S" first="Stefano" last="Barabino">Stefano Barabino</name>
<name sortKey="Dana, M Reza" sort="Dana, M Reza" uniqKey="Dana M" first="M. Reza" last="Dana">M. Reza Dana</name>
<name sortKey="De Fougerolles, Antonin R" sort="De Fougerolles, Antonin R" uniqKey="De Fougerolles A" first="Antonin R." last="De Fougerolles">Antonin R. De Fougerolles</name>
<name sortKey="Gardner, Humphrey" sort="Gardner, Humphrey" uniqKey="Gardner H" first="Humphrey" last="Gardner">Humphrey Gardner</name>
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</country>
</tree>
</affiliations>
</record>
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