DNA from Mycobacterium bovis bacillus Calmette-Guérin (MY-1) inhibits immunoglobulin E production by human lymphocytes.
DNA from Mycobacterium bovis bacillus Calmette-Guérin (MY-1) inhibits immunoglobulin E production by human lymphocytes.
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DOI：
10.1164/ajrccm.160.6.9903008
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发表时间：
1999-12
影响因子：
24.7
通讯作者：
S. Fujieda;S. Iho;Y. Kimura;H. Sunaga;H. Igawa;C. Sugimoto;Saburo Yamamoto;Hitoshi Saito
中科院分区：
文献类型：
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作者：
S. Fujieda;S. Iho;Y. Kimura;H. Sunaga;H. Igawa;C. Sugimoto;Saburo Yamamoto;Hitoshi Saito
从牛分枝杆菌卡介苗（BCG）中纯化的DNA组分，命名为MY-1诱导人外周血单核细胞（PBMC）产生干扰素（IFN）-γ。IFN-γ是众所周知的IgE产生的下调因子。在这项研究中，我们研究了MY-1是否调节IgE的生产，由人PBMC在体外。MY-1可抑制正常人外周血单个核细胞（PBMC）在白细胞介素（IL）-4和抗CD 40单克隆抗体刺激下产生IgE，但不影响伊加的产生。MY-1增强PBMC产生IFN-γ和IL-12。MY-1对IgE产生的抑制作用由IFN-γ和IL-12介导，因为MY-1诱导的抑制作用可通过添加单克隆抗IFN-γ抗体、单克隆抗IL-12抗体或针对IL-12受体的单克隆抗体（mAb）来阻断。MY-1抑制IL-4诱导人胚系转录。此外，MY-1在不存在IL-4加抗CD 40 mAb的情况下抑制来自特应性供体的PBMC体外自发产生IgE。这些结果表明，暴露于MY-1可能是治疗IgE相关过敏性疾病的一种新策略。
A DNA fraction purified from Mycobacterium bovis bacillus Calmette-Guérin (BCG) and designated MY-1 induced interferon (IFN)-gamma production by human peripheral blood mononuclear cells (PBMC). IFN-gamma is well known as a downregulator of IgE production. In this study we investigated whether MY-1 regulates IgE production by human PBMC in vitro. MY-1 inhibited IgE production in PBMC taken from normal donors and stimulated with interleukin (IL)-4 plus monoclonal anti-CD40 antibody, without affecting production of IgA. MY-1 enhanced production of IFN-gamma and IL-12 by PBMC. Inhibition by MY-1 of IgE production was mediated by both IFN-gamma and IL-12, since the MY-1-induced suppression was blocked by the addition of monoclonal anti-IFN-gamma antibody, monoclonal anti-IL-12 antibody or a monoclonal antibody (mAb) directed at the IL-12 receptor. MY-1 inhibited the induction of epsilon germ-line transcript by IL-4. Additionally, MY-1 inhibited spontaneous in vitro production of IgE by PBMC from atopic donors in the absence of IL-4 plus anti-CD40 mAb. These results suggest that exposure to MY-1 may be a novel strategy for the treatment of IgE-related allergic disease.