Sharma Monal, Webber S A, Zeevi A, Mohanakumar T
Norton Thoracic Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, United States.
Vanderbilt University School of Medicine, Nashville, TN, United States.
Hum Immunol. 2019 Apr;80(4):248-256. doi: 10.1016/j.humimm.2019.01.008. Epub 2019 Jan 30.
Antibodies to HLA resulting in positive cytotoxicity crossmatch are generally considered a contraindication for cardiac transplantation. However, cardiac transplantations have been performed in children by reducing the Abs and modifying immunosuppression. To identify mechanisms leading to allograft acceptance in the presence of Abs to donor HLA, we analyzed priming events in endothelial cells (EC) by incubating with sera containing low levels of anti-HLA followed by saturating concentration of anti-HLA. Pre-transplant sera were obtained from children with low levels of Abs to HLA who underwent transplantation. EC were selected for donor HLA and exposed to sera for 72 h (priming), followed by saturating concentrations of anti-HLA (challenge). Priming of EC with sera induced the phosphatidylinositol 3-kinase/Akt mediated by the BMP4/WNT pathway and subsequent challenge with panel reactive antibody sera increased survival genes Bcl2 and Heme oxygenase-1, decreased adhesion molecules, induced complement inhibitory proteins and reduced pro-inflammatory cytokines. In contrast, EC which did not express donor HLA showed decreased anti-apoptotic genes. Primed EC, upon challenge with anti-HLA, results in increased survival genes, decreased adhesion molecules, induction of complement inhibitory proteins, and downregulation of pro-inflammatory cytokines which may result in accommodation of pediatric cardiac allografts despite HLA sensitization.
导致细胞毒性交叉配型阳性的抗人白细胞抗原(HLA)抗体通常被视为心脏移植的禁忌证。然而,通过降低抗体水平和调整免疫抑制方案,儿童心脏移植手术仍得以开展。为了确定在存在供体HLA抗体的情况下导致同种异体移植物被接受的机制,我们通过用含有低水平抗HLA的血清孵育内皮细胞(EC),随后加入饱和浓度的抗HLA,来分析内皮细胞中的启动事件。移植前血清取自接受移植的、抗HLA抗体水平较低的儿童。选择表达供体HLA的内皮细胞并使其暴露于血清中72小时(启动),随后加入饱和浓度的抗HLA(激发)。用血清启动内皮细胞可诱导由骨形态发生蛋白4(BMP4)/Wnt信号通路介导的磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt),随后用群体反应性抗体血清激发可增加存活基因Bcl-2和血红素加氧酶-1(HO-1)的表达,减少黏附分子,诱导补体抑制蛋白并降低促炎细胞因子水平。相比之下,不表达供体HLA的内皮细胞显示抗凋亡基因减少。用抗HLA激发经启动的内皮细胞,可导致存活基因增加、黏附分子减少、补体抑制蛋白的诱导以及促炎细胞因子的下调,这可能导致小儿心脏同种异体移植物尽管存在HLA致敏仍能被容纳。