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Donor CCR5 Delta32 polymorphism and outcome following cardiac transplantation.

Authors :
Fildes JE
Walker AH
Howlett R
Bittar MN
Hutchinson IV
Leonard CT
Yonan N
Source :
Transplantation proceedings [Transplant Proc] 2005 Jun; Vol. 37 (5), pp. 2247-9.
Publication Year :
2005

Abstract

Background: Chemokines regulate the recruitment and trafficking of leukocytes during an immune response. Animal models have shown correlations between chemokine production and leukocyte infiltration during allograft rejection. Also, antagonism of chemokine receptors in transplant models has produced prolonged graft survival. Individuals homozygous for a 32 base pair deletion in the CC chemokine receptor 5 (CCR5) gene have an inactive receptor. Renal transplant recipients homozygous for the deletion have been shown to survive significantly longer than those heterozygous or homozygous for the wild type allele. CCR5 ligands are upregulated during allograft rejection aiding infiltration of leukocytes. We investigated the influence of CCR5Delta32 polymorphism on outcome following human cardiac transplantation.<br />Methods: Recipients and corresponding donors were genotyped for CCR5Delta32 polymorphism using polymerase chain reactions.<br />Results: We found no correlation between recipient genotype and outcome following transplantation. However, there was a significant correlation between donor genotype and mortality in patients transplanted for a nonischemic condition (DD = n/a, ID = 4%, II = 25%, P = .0014).<br />Conclusions: The induction of CCR5 expression in endomyocardial biopsy tissue is known to correlate with leukocyte graft infiltration. We suggest that donor CCR5 may be more important for leukocyte trafficking during rejection than recipient CCR5 expression. The CCR5 gene is highly conserved, and due to the small population available for this study, more work is required from other centers.

Details

Language :
English
ISSN :
0041-1345
Volume :
37
Issue :
5
Database :
MEDLINE
Journal :
Transplantation proceedings
Publication Type :
Academic Journal
Accession number :
15964389
Full Text :
https://doi.org/10.1016/j.transproceed.2005.03.101