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静脉注射丙种球蛋白对川崎病体内淋巴细胞活化的逆转作用。

Reversal of lymphocyte activation in vivo in the Kawasaki syndrome by intravenous gammaglobulin.

作者信息

Leung D Y, Burns J C, Newburger J W, Geha R S

出版信息

J Clin Invest. 1987 Feb;79(2):468-72. doi: 10.1172/JCI112835.

DOI:10.1172/JCI112835
PMID:2433307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC424104/
Abstract

The effect of intravenous gammaglobulin (IVGG) on the immunoregulatory abnormalities found during acute Kawasaki syndrome (KS) was studied in a randomized trial of IVGG plus aspirin (ASA) versus ASA alone. Before therapy, patients in each treatment group had increased numbers of circulating HLA-DR-bearing Leu 3+ helper T cells, a deficiency of Leu 2+ suppressor/cytotoxic T cells, and increased levels of spontaneous IgG and IgM synthesis by peripheral blood mononuclear cells. There were no significant differences (P greater than 0.1) between immunologic parameters measured on day 1 and day 4 in the ASA-treated group. In contrast, patients treated with ASA plus IVGG had by day 4 a highly significant decrease in HLA-Dr+ Leu 3+ helper T cells (P less than 0.001), an increase in Leu 2+ suppressor/cytotoxic T cells (P less than 0.01), and a decrease in spontaneous IgG (P less than 0.01) and IgM synthesis (P less than 0.001). These changes were associated with a reduction in the secretion of T cell-derived B cell helper factors (P less than 0.001). These findings indicate that treatment with IVGG suppresses the marked T and B cell activation found in patients with acute KS.

摘要

在一项静脉注射丙种球蛋白(IVGG)加阿司匹林(ASA)与单用阿司匹林的随机试验中,研究了静脉注射丙种球蛋白对急性川崎综合征(KS)期间发现的免疫调节异常的影响。治疗前,每个治疗组的患者循环中携带HLA-DR的Leu 3 +辅助性T细胞数量增加,Leu 2 +抑制/细胞毒性T细胞缺乏,外周血单个核细胞自发合成IgG和IgM的水平升高。在ASA治疗组中,第1天和第4天测量的免疫参数之间无显著差异(P大于0.1)。相比之下,接受ASA加IVGG治疗的患者到第4天时,HLA-Dr + Leu 3 +辅助性T细胞显著减少(P小于0.001),Leu 2 +抑制/细胞毒性T细胞增加(P小于0.01),自发IgG(P小于0.01)和IgM合成减少(P小于0.001)。这些变化与T细胞衍生的B细胞辅助因子分泌减少有关(P小于0.001)。这些发现表明,IVGG治疗可抑制急性KS患者中明显的T和B细胞活化。

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本文引用的文献

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Lancet. 1984 Nov 10;2(8411):1055-8. doi: 10.1016/s0140-6736(84)91504-6.
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Immune interferon produced to high levels by antigenic stimulation of human lymphocytes with influenza virus.通过用流感病毒对抗人淋巴细胞进行抗原刺激可产生高水平的免疫干扰素。
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Dysfunctions of pokeweed mitogen-stimulated T and B lymphocyte responses induced by gammaglobulin therapy.丙种球蛋白治疗诱导的商陆有丝分裂原刺激的T和B淋巴细胞反应功能障碍。
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