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特发性门脉高压(IPH)的病因学仍不明了。很多报道认为IPH与各种自身免疫性疾病有关。自身免疫性疾病中的高γ-球蛋白血症和各种自身抗体的产生被认为由T细胞调节B细胞的异常引起。T淋巴细胞与自身非-T淋巴细胞培养时的增生反应称自身混合性淋巴细胞反应(AMLR)。作者分析了IPH患者脾和周围血淋巴细胞的AMLR活性。材料与方法:受测的3例IPH患者均有门脉高压,但无肝硬化,无甲状腺功能异常,也未测出自身抗体。同时以6名健康人和1例脾破裂者作对照。1.纯化T细胞和非-T细胞:分别采集患者和健康人静脉血各50ml。切下脾脏经分离、过滤去除结缔组织,离心取得单
The etiology of idiopathic portal hypertension (IPH) remains unclear. Many reports suggest that IPH is associated with various autoimmune diseases. Hypergammaglobulinemia and the production of various autoantibodies in autoimmune diseases are thought to be caused by T cell-mediated abnormalities of B cells. The proliferative response of T lymphocytes to their own non-T lymphocytes is called autologous mixed lymphocyte reaction (AMLR). The authors analyzed AMLR activity in spleen and peripheral blood lymphocytes in patients with IPH. MATERIALS AND METHODS: Three patients with IPH underwent portal hypertension without cirrhosis, no thyroid dysfunction and no autoantibodies. At the same time to 6 healthy people and 1 case of splenic rupture as control. 1. Purified T cells and non-T cells: Separately collect 50ml of venous blood from each of healthy and healthy people. Cut off the spleen by filtration, remove the connective tissue, centrifuged to obtain a single