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复发性自然流产患者免疫治疗的一种可能机制。

A possible mechanism of immunotherapy for patients with recurrent spontaneous abortions.

作者信息

Sugi T, Makino T, Maruyama T, Kim W K, Iizuka R

机构信息

Department of Obstetrics and Gynecology, School of Medicine, Keio University, Tokyo, Japan.

出版信息

Am J Reprod Immunol. 1991 May;25(4):185-9. doi: 10.1111/j.1600-0897.1991.tb01092.x.

Abstract

The mechanism of the beneficial effect of immunotherapy for human reproductive wastage remains to be elucidated. Induction of blocking antibodies such as anti-HLA class II antibodies and anti-idiotypic antibodies was investigated as the mechanism of specific immunosuppression in pregnancy. We reported the changes in the mixed lymphocyte reaction (MLR), T-cell subsets, and generation of anti-idiotypic antibodies after immunotherapy compared to before immunotherapy. MLR was significantly (P less than 0.001) inhibited after the immunization. The mean inhibition rate was 50.2%, suggesting that MLR blocking antibodies were induced by immunotherapy. Binding of autoantibodies to alloactivated maternal lymphoblasts against the paternal lymphocytes was detected in postimmunization cases in two-color flow-cytometric experiments. This suggests that anti-idiotypic antibodies were induced by the immunotherapy. The percentage of cytotoxic T-cells was significantly decreased (P less than 0.05) and the percentage of suppressor T-cells was significantly increased (P less than 0.01) after the immunotherapy, suggesting that a cell-mediated immune response was induced by the immunotherapy.

摘要

免疫疗法对人类生殖损耗有益作用的机制仍有待阐明。作为孕期特异性免疫抑制的机制,对诸如抗II类人白细胞抗原抗体和抗独特型抗体等封闭抗体的诱导进行了研究。我们报告了与免疫疗法前相比,免疫疗法后混合淋巴细胞反应(MLR)、T细胞亚群及抗独特型抗体生成的变化。免疫后MLR受到显著抑制(P<0.001)。平均抑制率为50.2%,提示免疫疗法诱导了MLR封闭抗体。在双色流式细胞术实验中,在免疫后病例中检测到自身抗体与针对父方淋巴细胞的同种异体活化母方淋巴母细胞的结合。这提示免疫疗法诱导了抗独特型抗体。免疫疗法后,细胞毒性T细胞百分比显著降低(P<0.05),抑制性T细胞百分比显著升高(P<0.01),提示免疫疗法诱导了细胞介导的免疫反应。

相似文献

6
Mixed maternal-paternal lymphocyte cultures before and after immunotherapy for recurrent spontaneous abortions.
Am J Reprod Immunol. 1996 Jan;35(1):30-3. doi: 10.1111/j.1600-0897.1996.tb00005.x.

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