Angaswamy N, Klein C, Tiriveedhi V, Gaut J, Anwar S, Rossi A, Phelan D, Wellen J R, Shenoy S, Chapman W C, Mohanakumar T
Department of Surgery, Washington University School of Medicine, St. Louis, MO.
Am J Transplant. 2014 Mar;14(3):685-93. doi: 10.1111/ajt.12592. Epub 2014 Jan 10.
Antibodies (Abs) to donor HLA (donor-specific antibodies [DSA]) have been associated with transplant glomerulopathy (TG) following kidney transplantation (KTx). Immune responses to tissue-restricted self-antigens (self-Ags) have been proposed to play a role in chronic rejection. We determined whether KTx with TG have immune responses to self-Ags, Collagen-IV (Col-IV) and fibronectin (FN). DSA were determined by solid phase assay, Abs against Col-IV and FN by enzyme-linked immunosorbent assay and CD4+ T cells secreting interferon gamma (IFN-γ), IL-17 or IL-10 by ELISPOT. Development of Abs to self-Ags following KTx increased the risk for TG with an odds ratio of 22 (p-value = 0.001). Abs to self-Ags were IgG and IgM isotypes. Pretransplant Abs to self-Ags increased the risk of TG (22% vs. 10%, p < 0.05). Abs to self-Ags were identified frequently in KTx with DSA. TG patients demonstrated increased Col-IV and FN specific CD4+ T cells secreting IFN-γ and IL-17 with reduction in IL-10. We conclude that development of Abs to self-Ags is a risk factor and having both DSA and Abs to self-Ags increases the risk for TG. The increased frequency of self-Ag-specific IFN-γ and IL-17 cells with reduction in IL-10 demonstrate tolerance breakdown to self-Ags which we propose play a role in the pathogenesis of TG.
肾移植(KTx)后,针对供体人类白细胞抗原的抗体(Abs,即供体特异性抗体[DSA])与移植肾小球病(TG)有关。有人提出,对组织限制性自身抗原(自身Ags)的免疫反应在慢性排斥反应中起作用。我们确定了患有TG的KTx患者是否对自身Ags、IV型胶原(Col-IV)和纤连蛋白(FN)有免疫反应。通过固相分析确定DSA,通过酶联免疫吸附测定确定抗Col-IV和FN的抗体,通过酶联免疫斑点法确定分泌干扰素γ(IFN-γ)、白细胞介素-17(IL-17)或白细胞介素-10(IL-10)的CD4+T细胞。KTx后出现针对自身Ags的抗体增加了发生TG的风险,比值比为22(p值=0.001)。针对自身Ags的抗体为IgG和IgM亚型。移植前针对自身Ags的抗体增加了发生TG的风险(22%对10%,p<0.05)。在有DSA的KTx中经常发现针对自身Ags的抗体。TG患者显示分泌IFN-γ和IL-17的Col-IV和FN特异性CD4+T细胞增加,而IL-10减少。我们得出结论,针对自身Ags的抗体的出现是一个危险因素,同时存在DSA和针对自身Ags的抗体增加了发生TG的风险。自身抗原特异性IFN-γ和IL-17细胞频率增加而IL-10减少表明对自身Ags的耐受破坏,我们认为这在TG的发病机制中起作用。