虽然在移植过程中补体（C）的沉积和移植物的排斥反应相关，但是该通路的具体机制尚未明确。此外，有证据表明补体介导的细胞溶解可能对于mAb疗法耐受诱导有关键作用。同时，我们还评估了经典的补体通路在移植物急性排斥反应及实验性mAb疗法的需要。C1q缺陷的受者(C1q-/-)相比与野生型受者(WT)排斥反应发生更快。这些排斥反应往往合并有移植物病理学恶化，但是在C1q-/-的受者中并没有出现T细胞增强的反应。但是，C1q-/-的小鼠对于供者同种抗原的体液反应则有所增强，因为我们观察到了早期IgG反应和移植物内IgG沉积。更进一步说， C1q-/-受者的移植物中出现了C3d的沉积，而不是C4d。为了评估经典的补体通路在mAb诱导治疗中的作用，C1q-/-受者采用抗-CD4或抗CD40L单抗。在C1q-/-受者中，抗CD4单抗的作用被减弱，但是该作用并不与CD4+细胞无效的耗竭相关。相比之下，抗CD40LmAb的保护作用在C1q-/-受者中则很少有减弱。因此，该研究提示C1q在排斥反应过程中有非预计的作用。

Though complement (C) deposition within the transplant is associated with allograft rejection, the pathways employed have not been established. In addition, evidence suggests that C-mediated cytolysis may be necessary for the tolerance-inducing activities of mAb therapies. Hence, we assessed the role of the classical C pathway in acute allograft rejection and its requirement for experimental mAb therapies. C1q-deficient (C1q-/-) recipients rejected allografts at a faster rate than wild-type (WT) recipients. This rejection was associated with exacerbated graft pathology but not with enhanced T-cell responses in C1q-/- recipients. However, the humoral response to donor alloantigens was accelerated in C1q-/- mice, as an early IgG response and IgG deposition within the graft were observed. Furthermore, deposition of C3d, but not C4d was observed in grafts isolated from C1q-/- recipients. To assess the role of the classical C pathway in inductive mAb therapies, C1q-/- recipients were treated with anti-CD4 or anti-CD40L mAb. The protective effects of anti-CD4 mAb were reduced in C1q-/- recipients, however, this effect did not correlate with ineffective depletion of CD4+ cells. In contrast, the protective effects of anti-CD40L mAb were less compromised in C1q-/- recipients. Hence, this study reveals unanticipated roles for C1q in the rejection process.