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J Thorac Cardiovasc Surg 2003;126:1251-1253
© 2003 The American Association for Thoracic Surgery

Editorials

Improving the allograft valve: does the immune response matter?

Patrick G. Hogan, MBBS, PhD, FRACP, FRCPA*,a, Mark F. O'Brien, MBBS, FRACSa

a Department of Clinical Immunology, Princess Alexandra Hospital, Woolloongabba, Brisbane, Australia

Received for publication April 16, 2003; accepted for publication April 24, 2003.

* Address for reprints: Patrick G. Hogan, PhD, Director, Division of Immunology, Queensland Health Pathology Service, Princess Alexandra Hospital, Ipswich Rd, Woolloongabba QLD Australia 4102
Patrick_Hogan@health.qld.gov.au

The first 20% of the full text of this article appears below.


See related article in 2003;126: 232-9.

 

Can an immunologic attack on cells expressing donor human leukocyte antigens (HLAs) contribute to human allograft valve (AV) deterioration? Not so, say the supporters of a mechanical mechanism of failure.1 They interpret anti-HLA antibodies in AV recipients2-4 as irrelevant epiphenomena that result from mechanical failure liberating soluble HLA from the AV to stimulate the immune system.5 Unfortunately, this hypothesis is inconsistent with the appearance of anti-HLA antibodies within 30 days of implantation.3 Nevertheless, until recently, a pathogenic role for the immune response in AV degeneration was unproved because a link with functional outcomes was lacking.

The report by Baskett and colleagues6 in the July 2003 issue, together with similar conclusions from Dignan and associates,7 provides convincing evidence that a significant component of AV degeneration is immunologic. What is the mechanism linking AV deterioration and HLA mismatch between donor and recipient? The same relationship is shown in extensive multicenter studies of solid organ transplants between 0 to 6 antigen HLA mismatches and solid organ graft failure rates.8 The accepted underlying mechanism is an allogeneic T-cell response initiated by recognition of nonself HLA-DR on graft dendritic and endothelial cells, followed by an amplification phase against HLA-A and . . . [Full Text of this Article]




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