INCREASED EXPRESSION OF MHC CLASS-II ANTIGENS IN REJECTING CANINE LUNG ALLOGRAFTS
INCREASED EXPRESSION OF MHC CLASS-II ANTIGENS IN REJECTING CANINE LUNG ALLOGRAFTS
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DOI：
10.1097/00007890-199006000-00026
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发表时间：
1990-06-01
期刊：
影响因子：
6.2
通讯作者：
LIN, CY
中科院分区：
文献类型：
--
作者：
CHANG, SC;HSU, HK;LIN, CY
单肺移植后，在正常肺和杂种犬的肺同种异体移植中研究了主要的组织相容性复合物II类抗原的表达。用间接免疫过氧化物酶技术将低温恒温器切片染色，该技术将B1F6和7.5.10.1用作抗MHC II类单克隆抗体。在单肺移植后，在受体犬的正常肺和天然肺中，仅一些淋巴组织和巨噬细胞/树突状细胞的细胞是MHC II类阳性。在急性排斥期间，在肺同种异体移植物中发现了血管周围，周围和间质区域中MHC II类阳性细胞的浸润增加。此外，在支气管上皮和血管内皮上诱导了MHC II类抗原的表达。在单肺移植后两天，发现了拒绝肺同种异体移植物在支气管上皮和血管内皮上的MHC II类抗原表达。移植肺中支气管上皮和血管内皮的MHC II类抗原表达的强度随反应反应的进展而增加，并且与支气管肺泡灌洗液（BALF）的生化标记水平直接相关，作为肿瘤坏死因子。干扰素（IFN-.gamma。），白介素2 （IL-2）和可溶性白介素2受体（SIL-2R）。 MHC II类抗原在支气管上皮和血管内皮上的异常表达以及肺同种异体移植中细胞因子水平的异常升高可以通过环孢素（CSA）治疗来预防。我们的结果表明，在急性排斥反应期间，可以在犬肺同种异体移植物的支气管上皮和血管内皮上诱导MHC II类抗原表达。当可能排除MHC II类抗原在支气管上皮和血管内皮上移植肺的血管内皮的异常表达，可以作为诊断肺同种异体移植作为诱导因子的特定指数。此外，肺同种异体移植物的支气管上皮和血管内皮已成为MHC II类阳性，并且可能是低度排斥反应的靶标，导致肺中支气管炎的发展，并在肺同种异体中发展了闭塞性血管疾病。
Expression of major histocompatibility complex class II antigens was investigated in the normal lungs and in lung allografts of mongrel dogs after single-lung transplantation. Cryostat sections were stained with an indirect immunoperoxidase technique that used B1F6 and 7.5.10.1 as anti-MHC class II monoclonal antibodies. In the normal lungs and native lungs of the recipient dogs after single-lung transplantation, only some cells of lymphoid tissue and macrophages/dendritic cells were MHC class II-positive. During acute rejection, increased infiltration with MHC class II-positive cells in perivascular, peribronchial, and interstitial areas and intraalveolar spaces was found in lung allografts. In addition, expression of MHC class II antigens was induced on the bronchial epiethelium and vascular endothelium. Induced expression of MHC class II antigens on the bronchial epithelium and vascular endothelium in rejecting lung allografts was found as early as two days after single-lung transplantation. The intensity of MHC class II antigen expression of bronchial epithelium and vascular endothelium in graft lungs increased with the progression of rejection response and directly correlated with the bronchoalveolar lavage fluid (BALF) levels of biochemical markers, as tumor necrosis factor .alpha., gamma-interferon (IFN-.gamma.), interleukin 2 (IL-2) and soluble interleukin 2 receptor (SIL-2R). Abnormal expression of MHC class II antigens on bronchial epithelium and vascular endothelium and abnormal elevation of BALF levels of the cytokines in lung allografts could be prevented by cyclosporine (CsA) treatment. Our results suggested that MHC class II antigen expression could be induced on the bronchial epithelium and vascular endothelium of canine lung allografts during acute rejection. This abnormal expression of MHC class II antigens on bronchial epithelium and vascular endothelium of graft lungs may serve as a specific index for diagnosis of lung allograft rejection when infection as an inducing factor can be excluded. Furthermore, bronchial epithelium and vascular endothelium of lung allografts have become MHC class II-positive, and are likely to be the targets for low-grade rejection, resulting in the development of bronchiolitis obliterans and occlusive vascular disease in lung allografts.