期刊
TRANSPLANTATION
卷 86, 期 9, 页码 1319-1321出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/TP.0b013e3181889831
关键词
Heart transplantation; Human; Complement; Gene expression
资金
- NIAID NIH HHS [U01 AI063594-05, U01 AI63594, R01 AI043578, U01 AI063594] Funding Source: Medline
Complement activation contributes to antibody-mediated allograft rejection, but increasing evidence also implicates complement proteins produced locally within the graft, in part by infiltrating mononuclear cells, as important mediators of tissue injury. To test this concept in transplant recipients, we evaluated complement, complement regulator, and T cell/proinflammatory marker gene expression by quantitative real-time polymerase chain reaction in 71 archived heart transplant biopsies and correlated the results with the histologic grade of rejection. Significantly more transcripts encoding alternative pathway components factor B, C3 and properdin, and C3a receptor and C5a receptor were detected in grade 3 versus grade 0 or I biopsies. The grade 3 rejections also contained significantly higher amounts of CD3, interferon gamma, perforin, and granzyme B genes. In addition to providing supportive evidence for a pathogenic role of graft-derived complement in human heart transplant injury, these correlations suggest that molecular profiling of complement gene expression could be useful in the diagnosis of human allograft rejection.
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