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B cell activation and Ig, especially IgE, production is inhibited by high CD23 levels in vivo and in vitro.在体内和体外,高CD23水平会抑制B细胞活化以及Ig尤其是IgE的产生。
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J Invest Dermatol. 1994 Mar;102(3):321-7. doi: 10.1111/1523-1747.ep12371790.
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Manipulation of Th1/Th2 balance in vivo by adoptive transfer of antigen-specific Th1 or Th2 cells.通过抗原特异性Th1或Th2细胞的过继转移在体内操纵Th1/Th2平衡。
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Antigen-specific memory in B-1a and its relationship to natural immunity.B-1a 细胞中的抗原特异性记忆及其与天然免疫的关系。
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Soluble CD23 controls IgE synthesis and homeostasis in human B cells.可溶性 CD23 控制人类 B 细胞中的 IgE 合成和动态平衡。
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GATA transcription factors are involved in IgE-dependent mast cell degranulation by enhancing the expression of phospholipase C-γ1.GATA 转录因子通过增强磷脂酶 C-γ1 的表达参与 IgE 依赖性肥大细胞脱颗粒。
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Schistosomes induce regulatory features in human and mouse CD1d(hi) B cells: inhibition of allergic inflammation by IL-10 and regulatory T cells.曼氏血吸虫诱导人源和鼠源 CD1d(hi)B 细胞呈现调节性特征:IL-10 和调节性 T 细胞抑制过敏炎症。
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In vitro diagnosis of IgE-mediated allergy: breakthroughs in the last decade.IgE介导的过敏症的体外诊断:过去十年的突破。
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Immunology in the Clinic Review Series; focus on allergies: immunotherapy for food allergy.临床免疫学评论系列;关注过敏:食物过敏的免疫疗法。
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The role of mast cells in allergic inflammation.肥大细胞在过敏炎症中的作用。
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Insights into the initiation of type 2 immune responses.对 2 型免疫应答起始的深入了解。
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9
Cytokine-induced alterations of α7 nicotinic receptor in colonic CD4 T cells mediate dichotomous response to nicotine in murine models of Th1/Th17- versus Th2-mediated colitis.细胞因子诱导的结肠 CD4 T 细胞α7 烟碱型乙酰胆碱受体的改变介导了 Th1/Th17 与 Th2 介导结肠炎小鼠模型对尼古丁的双重反应。
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Mechanisms of immunotherapy to aeroallergens.免疫疗法治疗气传过敏原的机制。
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抗原特异性免疫疗法调节肠道中的 B 细胞活性。

Antigen-specific immunotherapy regulates B cell activities in the intestine.

机构信息

Department of Geriatrics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

Department of Orthopedics, First Affiliated Hospital of Chongqing Medical University, Chongqing 40016, China.

出版信息

J Biol Chem. 2013 Jun 7;288(23):16383-16390. doi: 10.1074/jbc.M113.456202. Epub 2013 Apr 15.

DOI:10.1074/jbc.M113.456202
PMID:23589293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3675575/
Abstract

Mature B cells (BCs) express CD23 and B cell receptors. Whether activation of CD23 and B cell receptors has different effects on BC activities is unclear. This study aims to investigate the mechanism by which the specific antigen immunotherapy regulates the activation of BCs in the skewed Th2 responses. Mice were sensitized to ovalbumin. The specific antigen vaccination (SAV) at graded doses was employed to modulate the activities of BCs in which the expression of IL-10, IgE, matrix metalloproteinase-9 (MMP9), CD23, and serum soluble CD23 by BCs was evaluated. The immune regulatory effect of BCs primed by lower or higher SAV doses was observed with an adoptive transfer mouse experiment. SAV activated CD23 to produce IL-10 in BCs at lower doses. The higher doses of SAV increased the expression of MMP9 in BCs that reduced the amounts of CD23 in BCs and increased the serum levels of soluble CD23, which was abrogated by the pretreatment with MMP9 inhibitor. Adoptively transfer with BCs primed by lower doses of SAV inhibited the ongoing antigen-specific Th2 responses whereas the BCs primed by higher doses of SAV exacerbated the ongoing Th2 responses. Exposure to specific antigens at optimal doses can activate BCs to produce IL-10 to suppress the skewed antigen-specific Th2 responses. The antigen doses of SAV higher than the optimal doses may promote the production of soluble CD23 to exacerbate the ongoing immune responses.

摘要

成熟 B 细胞 (BC) 表达 CD23 和 B 细胞受体。CD23 和 B 细胞受体的激活是否对 BC 活性有不同的影响尚不清楚。本研究旨在探讨特异性抗原免疫治疗调节偏倚 Th2 反应中 BC 激活的机制。用卵清蛋白致敏小鼠。采用分级剂量的特异性抗原疫苗接种 (SAV) 来调节 BC 活性,评估 IL-10、IgE、基质金属蛋白酶-9 (MMP9)、CD23 和血清可溶性 CD23 的表达。通过过继转移小鼠实验观察了低剂量或高剂量 SAV 激活的 BC 的免疫调节作用。SAV 在低剂量下激活 CD23 以在 BC 中产生 IL-10。更高剂量的 SAV 增加了 MMP9 在 BC 中的表达,降低了 BC 中的 CD23 含量,并增加了血清可溶性 CD23 的水平,这被 MMP9 抑制剂预处理所阻断。用低剂量 SAV 预激活的 BC 过继转移抑制了正在进行的抗原特异性 Th2 反应,而用高剂量 SAV 预激活的 BC 加剧了正在进行的 Th2 反应。暴露于最佳剂量的特异性抗原可激活 BC 产生 IL-10 来抑制偏倚的抗原特异性 Th2 反应。高于最佳剂量的 SAV 抗原剂量可能会促进可溶性 CD23 的产生,从而加剧正在进行的免疫反应。