补体活活能够导致抗体介导的移植物排斥反应，但是有越来越多的证据表明移植物局部浸润的单核细胞产生的补体蛋白同样是组织损伤的重要介导物质。为了明确移植受者中该理论的正确性，我们采用RT-PCR的方法检测了71例心脏移植物活检标本中补体、补体调节物以及T细胞/促炎症反应标记物基因表达及其与排斥反应的组织学分级的相关程度。3级的排斥反应相比于0或者1级的排斥反应其活检标本中旁路途径成分因子B、C3以及备解素和C3a与C5a的受体表达均明显升高。3级排斥分那英同样存在更多的CD3、IFN-gamma、穿孔素和颗粒酶B基因的表达。这些相关性能够证明心脏移植物损伤中供者来源补体的病理性作用，还认为补体基因表达的分子特征在诊断人类移植物排斥反应中有用。

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 1 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.