The Role of Donor-Specific HLA Alloantibodies in Liver Transplantation
Identifieur interne : 000F73 ( Pmc/Curation ); précédent : 000F72; suivant : 000F74The Role of Donor-Specific HLA Alloantibodies in Liver Transplantation
Auteurs : J. G. O Eary [États-Unis] ; A. J. Demetris [États-Unis] ; L. S. Friedman [États-Unis] ; H. M. Gebel [États-Unis] ; P. F. Halloran [Canada] ; A. D. Kirk [États-Unis] ; S. J. Knechtle [États-Unis] ; S. V. Mcdiarmid [États-Unis] ; A. Shaked [États-Unis] ; P. I. Terasaki [États-Unis] ; K. J. Tinckam [Canada] ; S. J. Tomlanovich [États-Unis] ; K. J. Wood [Royaume-Uni] ; E. S. Woodle [États-Unis] ; A. A. Zachary [États-Unis] ; G. B. Klintmalm [États-Unis]Source :
- American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons [ 1600-6135 ] ; 2014.
Abstract
The impact of donor-specific HLA alloantibodies (DSA) on short- and long-term liver transplant outcome is not clearly defined. While it is clear that not all levels of allosensitization produce overt clinical injury, and that liver allografts possess some degree of alloantibody resistance, alloantibody-mediated adverse consequences are increasingly being recognized. To better define the current state of this topic, we assembled experts to provide insights, explore controversies and develop recommendations for future research on the consequences of DSA in liver transplantation. This article summarizes the proceedings of this inaugural meeting.
Several insights emerged. Acute antibody-mediated rejection (AMR), although rarely diagnosed, is increasingly understood to overlap with T cell–mediated rejection. Isolated liver allograft recipients are at increased risk of early allograft immunologic injury when preformed DSA are high titer and persist posttransplantation. Persons who undergo simultaneous liver–kidney transplantation are at risk of renal AMR when Class II DSA persist posttransplantation. Other under-appreciated DSA associations include ductopenia and fibrosis, plasma cell hepatitis, biliary strictures and accelerated fibrosis associated with recurrent liver disease. Standardized DSA testing and diagnostic criteria for both acute and chronic AMR are needed to distil existing associations into etiological processes in order to develop responsive therapeutic strategies.
Url:
DOI: 10.1111/ajt.12667
PubMed: 24580828
PubMed Central: 4412601
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<front><div type="abstract" xml:lang="en"><p id="P1">The impact of donor-specific HLA alloantibodies (DSA) on short- and long-term liver transplant outcome is not clearly defined. While it is clear that not all levels of allosensitization produce overt clinical injury, and that liver allografts possess some degree of alloantibody resistance, alloantibody-mediated adverse consequences are increasingly being recognized. To better define the current state of this topic, we assembled experts to provide insights, explore controversies and develop recommendations for future research on the consequences of DSA in liver transplantation. This article summarizes the proceedings of this inaugural meeting.</p>
<p id="P2">Several insights emerged. Acute antibody-mediated rejection (AMR), although rarely diagnosed, is increasingly understood to overlap with T cell–mediated rejection. Isolated liver allograft recipients are at increased risk of early allograft immunologic injury when preformed DSA are high titer and persist posttransplantation. Persons who undergo simultaneous liver–kidney transplantation are at risk of renal AMR when Class II DSA persist posttransplantation. Other under-appreciated DSA associations include ductopenia and fibrosis, plasma cell hepatitis, biliary strictures and accelerated fibrosis associated with recurrent liver disease. Standardized DSA testing and diagnostic criteria for both acute and chronic AMR are needed to distil existing associations into etiological processes in order to develop responsive therapeutic strategies.</p>
</div>
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<title-group><article-title>The Role of Donor-Specific HLA Alloantibodies in Liver Transplantation</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>O’Leary</surname>
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<given-names>S. V.</given-names>
</name>
<xref ref-type="aff" rid="A7">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Shaked</surname>
<given-names>A.</given-names>
</name>
<xref ref-type="aff" rid="A8">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Terasaki</surname>
<given-names>P. I.</given-names>
</name>
<xref ref-type="aff" rid="A9">9</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tinckam</surname>
<given-names>K. J.</given-names>
</name>
<xref ref-type="aff" rid="A10">10</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tomlanovich</surname>
<given-names>S. J.</given-names>
</name>
<xref ref-type="aff" rid="A11">11</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wood</surname>
<given-names>K. J.</given-names>
</name>
<xref ref-type="aff" rid="A12">12</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Woodle</surname>
<given-names>E. S.</given-names>
</name>
<xref ref-type="aff" rid="A13">13</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zachary</surname>
<given-names>A. A.</given-names>
</name>
<xref ref-type="aff" rid="A14">14</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Klintmalm</surname>
<given-names>G. B.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Annette C. and Harold C. Simmons Transplant Institute, Baylor University Medical Center, Dallas, TX</aff>
<aff id="A2"><label>2</label>
Department of Pathology, University of Pittsburgh, Pittsburgh, PA</aff>
<aff id="A3"><label>3</label>
Department of Medicine, Newton-Wellesley Hospital, Newton, MA</aff>
<aff id="A4"><label>4</label>
Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA</aff>
<aff id="A5"><label>5</label>
Transplant Applied Genomics Centre, University of Alberta, Edmonton, AB, Canada</aff>
<aff id="A6"><label>6</label>
Department of Surgery, Emory University, Atlanta, GA</aff>
<aff id="A7"><label>7</label>
Pediatric Transplantation, University of California, Los Angeles, Los Angeles, CA</aff>
<aff id="A8"><label>8</label>
Department of Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA</aff>
<aff id="A9"><label>9</label>
Terasaki Foundation Laboratory, Los Angeles, CA</aff>
<aff id="A10"><label>10</label>
Histocompatibility Laboratory, University Health Network, Toronto, ON, Canada</aff>
<aff id="A11"><label>11</label>
Pancreas Transplant Services, University of California, San Francisco, San Francisco, CA</aff>
<aff id="A12"><label>12</label>
Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK</aff>
<aff id="A13"><label>13</label>
Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, OH</aff>
<aff id="A14"><label>14</label>
Immunogenetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD</aff>
<author-notes><corresp id="FN1"><label>*</label>
Corresponding author: Jacqueline G. O’Leary, <email>jacquelo@baylorhealth.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>21</day>
<month>4</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>01</day>
<month>3</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="ppub"><month>4</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>28</day>
<month>4</month>
<year>2015</year>
</pub-date>
<volume>14</volume>
<issue>4</issue>
<fpage>779</fpage>
<lpage>787</lpage>
<pmc-comment>elocation-id from pubmed: 10.1111/ajt.12667</pmc-comment>
<abstract><p id="P1">The impact of donor-specific HLA alloantibodies (DSA) on short- and long-term liver transplant outcome is not clearly defined. While it is clear that not all levels of allosensitization produce overt clinical injury, and that liver allografts possess some degree of alloantibody resistance, alloantibody-mediated adverse consequences are increasingly being recognized. To better define the current state of this topic, we assembled experts to provide insights, explore controversies and develop recommendations for future research on the consequences of DSA in liver transplantation. This article summarizes the proceedings of this inaugural meeting.</p>
<p id="P2">Several insights emerged. Acute antibody-mediated rejection (AMR), although rarely diagnosed, is increasingly understood to overlap with T cell–mediated rejection. Isolated liver allograft recipients are at increased risk of early allograft immunologic injury when preformed DSA are high titer and persist posttransplantation. Persons who undergo simultaneous liver–kidney transplantation are at risk of renal AMR when Class II DSA persist posttransplantation. Other under-appreciated DSA associations include ductopenia and fibrosis, plasma cell hepatitis, biliary strictures and accelerated fibrosis associated with recurrent liver disease. Standardized DSA testing and diagnostic criteria for both acute and chronic AMR are needed to distil existing associations into etiological processes in order to develop responsive therapeutic strategies.</p>
</abstract>
<kwd-group><kwd>Antibody-mediated rejection</kwd>
<kwd>donor-specific HLA antibodies</kwd>
<kwd>graft outcomes</kwd>
<kwd>liver transplant</kwd>
<kwd>renal transplant</kwd>
<kwd>simultaneous liver–kidney transplant</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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