Anti-intercellular adhesion molecule-1 antibodies in sera of heart transplant recipients: A role in endothelial cell activation
Transplantation, ISSN: 0041-1337, Vol: 80, Issue: 2, Page: 264-271
2005
- 29Citations
- 16Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations29
- Citation Indexes29
- 29
- CrossRef24
- Captures16
- Readers16
- 16
Article Description
Background. Antiendothelial antibodies to non-human leukocyte antigens are made by a subset of heart transplant recipients, but the specificity of such antibodies is undefined. Intercellular adhesion molecule (ICAM)-1 is an abundantly expressed adhesion molecule with polymorphic residues, expressed on the surface of endothelial cells. The hypothesis that ICAM-1 acts as a minor histocompatibility antigen and that anti-ICAM-1 antibodies, directed against polymorphic residues, could be one component of the antiendothelial antibodies found after heart transplantation has been tested. Methods. Chinese hamster ovary cells were transfected with full-length polymorphic variants of human ICAM-1. The binding of antibodies (immunoglobulin [Ig] G or IgM) to these cells was measured using sera from 50 heart transplant recipients (pretransplant and 1 and 2 years posttransplant) and sera from 20 normal volunteers by flow cytometry. The recipients and donors were genotyped for ICAM-1 polymorphisms. Results. Sixty-eight percent (n=34) of patients made IgM antibodies that bound to ICAM-1. However, it seems unlikely that ICAM-1 is a minor transplantation antigen, because there were no differences in antibody production from recipients matched or mismatched for ICAM-1 alleles. The antibodies bound to mouse endothelial cells that were engineered to overexpress human ICAM-1, and induced a robust activation of the Erk-2 mitogen-activated protein kinase pathway. Conclusions. Anti-ICAM-1 antibodies are produced after cardiac transplantation, but not to polymorphic residues. Such antibodies may contribute to the endothelial activation by binding to the endothelium, causing activation of proinflammatory signaling pathways. Copyright © 2005 by Lippincott Williams & Wilkins.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=23044485917&origin=inward; http://dx.doi.org/10.1097/01.tp.0000165433.88295.4c; http://www.ncbi.nlm.nih.gov/pubmed/16041273; https://journals.lww.com/00007890-200507270-00016; http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00007890-200507270-00016; https://dx.doi.org/10.1097/01.tp.0000165433.88295.4c; https://journals.lww.com/transplantjournal/Fulltext/2005/07270/Anti_Intercellular_Adhesion_Molecule_1_Antibodies.16.aspx
Ovid Technologies (Wolters Kluwer Health)
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