Development of Elisa-Detected Anti-Hla Antibodies Precedes the Development of Bronchiolitis Obliterans Syndrome and Correlates With Progressive Decline in Pulmonary Function After Lung Transplantation1

Jaramillo, Andrés; Smith, Michael A.; Phelan, D.; Sundaresan, Sudhir; Trulock, Elbert P.; Lynch, John P.; Cooper, Joel D.; Patterson, G. Alexander; Mohanakumar, Thalachallour

doi:10.1097/00007890-199904270-00012

Cited by 179 publications

(131 citation statements)

References 24 publications

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“…Previous studies suggested a role for HLA antibodies after lung transplantation. [5][6][7][8]22,23 Girnita et al found that HLA antibodies are associated with increased frequency and more severe acute rejections after lung transplant, 5 as well as increased incidence of BOS. 6 Their studies had small patient cohorts and, although they used solid-phase antibody assays for HLA antibody detection, they were enzyme-linked immunoassay (ELISA)-based and, as such, probably underestimated the level of HLA antibody production.…”

Section: Discussionmentioning

confidence: 99%

De novo donor HLA-specific antibodies predict development of bronchiolitis obliterans syndrome after lung transplantation

Safavi

Robinson

Soresi

et al. 2014

The Journal of Heart and Lung Transplantation

111

102

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(2014) De novo donor HLA-specific antibodies predict development of bronchiolitis obliterans syndrome after lung transplantation. The Journal of Heart and Lung Transplantation, 33 (12). pp. 1273 -1281 . ISSN 1053 -2498 This version is available from Sussex Research Online: http://sro.sussex.ac.uk/56766/ This document is made available in accordance with publisher policies and may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the URL above for details on accessing the published version. Copyright and reuse:Sussex Research Online is a digital repository of the research output of the University.Copyright and all moral rights to the version of the paper presented here belong to the individual author(s) and/or other copyright owners. To the extent reasonable and practicable, the material made available in SRO has been checked for eligibility before being made available.Copies of full text items generally can be reproduced, displayed or performed and given to third parties in any format or medium for personal research or study, educational, or not-for-profit purposes without prior permission or charge, provided that the authors, title and full bibliographic details are credited, a hyperlink and/or URL is given for the original metadata page and the content is not changed in any way. There was a significant reduction in patient survival associated with de novo DSA (HR ¼ 1.886, p ¼ 0.047). In multivariable analyses, de novo DSA was an independent predictor for development of all stages of BOS as well as an independent predictor of poor patient survival. CONCLUSIONS: De novo DSA is a major risk factor for progression to BOS and shorter patient survival. Treatments to remove antibodies or limit antibody-mediated damage could be considered when DSA are first detected. However, a randomized, controlled trial of treatment options would enable a clearer understanding of the benefits, if any, of antibody-removal therapies.

show abstract

Section: Discussionmentioning

confidence: 99%

De novo donor HLA-specific antibodies predict development of bronchiolitis obliterans syndrome after lung transplantation

Safavi

Robinson

Soresi

et al. 2014

The Journal of Heart and Lung Transplantation

111

102

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“…For instance, increased post transplantation ventilator days, decreased survival and/or a higher incidence of BOOP were observed in patients with PRAs (8,9). Many studies have closely linked HLA antibodies to humoral allograft rejection (7,10).…”

Section: Discussionmentioning

confidence: 99%

“…As outlined by Pelletier et al (7)(8)(9)(10), a commercially available pool of microparticle beads coated with various purified MHC antigens of known specificity were used according to manufacturer's instructions (FlowPRA, OneLambda, Canoga Park, CA). Briefly, 20 lL of recipient sera was incubated with 5 lL of MHC Class I plus 5 lL of MHC Class II microparticle beads for 30 min at room temperature (RT).…”

Section: Flow Cytometric Alloantibody Detectionmentioning

confidence: 99%

Evidence That Humoral Allograft Rejection in Lung Transplant Patients Is Not Histocompatibility Antigen-Related

Magro¹,

Klinger²,

Adams³

et al. 2003

American Journal of Transplantation

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We have recently recognized humoral rejection (HR) in lung allograft recipients and its association with acute and chronic graft dysfunction. We have shown that C4d, a stable marker of classic complement activation, is deposited in lung allografts, correlating with clinical rejection and parenchymal injury. The antigenic target may be endothelium in the setting of recurrent acute rejection while varying components of the bronchial wall may be important in chronic graft dysfunction. We sought to establish whether there is a role for antibodies with histocompatibility antigen specificity in the lung humoral allograft phenomenon. Flow cytometric and ELISA assays to assess donor-specific antigens were conducted on sera from 25 lung transplant recipients who had experienced one or more episodes of clinical rejection; in addition, the serum samples were tested for evidence of antiendothelial cell antibody activity. Morphologically, each case had biopsies showing septal capillary injury with significant deposits of immunoreactants with microvascular localization and positive indirect immunofluorescent antiendothelial cell antibody assay. Panel-reactive antibody testing showed absence of MHC Class I/II alloantibodies; ELISA based crossmatch detecting donor-specific MHC Class I/II specific antibodies was negative. HR can occur in the absence of antibodies with HLA specificity; antigenic targets may be of endothelial cell origin.

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“…Elicitation of immune responses to the mismatched donor human leukocyte antigen (HLA) and breakdown of tolerance to tissue-restricted self-antigens pose a significant challenge to acceptance and continued graft function following organ transplantation (67,68). While the mechanisms of AMR are not firmly established, de novo donor-specific antibodies against HLA have been shown to predispose to the development of immune responses to lung self-antigens and BOS (69)(70)(71). To define mechanisms leading to anti-MHC-mediated development of rejection, a preclinical murine model was developed in which exogenous anti-MHC was administered into the native lungs and elicited production of antibodies and T cell responses specific for lung-associated self-antigens, type V collagen [col(V)], and K-α 1 tubulin, culminating in fibrotic pathology (72,73).…”

Section: Armentioning

confidence: 99%

Models of Lung Transplant Research: a consensus statement from the National Heart, Lung, and Blood Institute workshop

Lama¹,

Belperio²,

Christie³

et al. 2017

JCI Insight

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Development of Elisa-Detected Anti-Hla Antibodies Precedes the Development of Bronchiolitis Obliterans Syndrome and Correlates With Progressive Decline in Pulmonary Function After Lung Transplantation1

Cited by 179 publications

References 24 publications

De novo donor HLA-specific antibodies predict development of bronchiolitis obliterans syndrome after lung transplantation

De novo donor HLA-specific antibodies predict development of bronchiolitis obliterans syndrome after lung transplantation

Evidence That Humoral Allograft Rejection in Lung Transplant Patients Is Not Histocompatibility Antigen-Related

Models of Lung Transplant Research: a consensus statement from the National Heart, Lung, and Blood Institute workshop

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