INDUCTION OF IGA1 AND IGA2 PRODUCTION IN IMMATURE HUMAN FETAL B-CELLS AND PRE-B CELLS BY VASOACTIVE-INTESTINAL-PEPTIDE
INDUCTION OF IGA1 AND IGA2 PRODUCTION IN IMMATURE HUMAN FETAL B-CELLS AND PRE-B CELLS BY VASOACTIVE-INTESTINAL-PEPTIDE
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DOI：
10.1182/blood.v85.8.2098.bloodjournal8582098
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发表时间：
1995-04-15
期刊：
影响因子：
20.3
通讯作者：
FUJIMOTO, M
中科院分区：
文献类型：
--
作者：
KIMATA, H;FUJIMOTO, M
我们研究了血管活性肠肽（VIP）对人胎儿B细胞和骨髓前B细胞中IgA1和IgA2生成的影响。用抗cd40单克隆抗体（MoAb）刺激sIgM（+）、CD19（+）胎儿B细胞，VIP诱导IgA1、IgA2和IgM的产生，而不诱导IgG1、IgG2、IgG3、IgG4或IgE的产生。抗cd40的MoAb + VIP还能诱导sIgM（-）、CD19（+）前b细胞产生IgA1、IgA2和IgM，并通过添加白细胞介素-7 （IL-7）增强。VIP的这种诱导是特异性的，因为抗cd40 MoAb与其他神经肽[即生长抑素（SOM）或P物质（SP）]没有作用，而且VIP拮抗剂特异性地阻断了这种诱导。此外，抗cd40 MoAb加上各种细胞因子，包括IL-1 β、IL-2、IL-3、IL-4、IL-5、IL-6、IL-10、转化生长因子β (tgf - β)、低分子B细胞生长因子（BCGF）和干扰素γ (ifn - γ)，不会诱导胎儿B细胞或前B细胞产生IgA1和IgA2。这些发现表明，在共刺激物存在的情况下，VIP可能通过同型转换诱导IgA1和IgA2的产生。(C) 1995年由美国血液病学会出版。
We studied the effects of vasoactive intestinal peptide (VIP) on IgA1 and IgA2 production in human fetal B cells and pre-B cells derived from bone marrow. VIP induced IgA1, IgA2, and IgM production in sIgM(+), CD19(+) fetal B cells stimulated with anti-CD40 monoclonal antibody (MoAb) without inducing the production of IgG1, IgG2, IgG3, IgG4, or IgE. The anti-CD40 MoAb plus VIP also induced IgA1, IgA2, and IgM production in sIgM(-), CD19(+) pre-B cells, which was enhanced by the addition of interleukin-7 (IL-7). This induction by VIP was specific, as the anti-CD40 MoAb plus other neuropeptides [ie, somatostatin (SOM) or substance P (SP)] had no effect, and moreover, the induction was specifically blocked by a VIP antagonist. Furthermore, the anti-CD40 MoAb plus various cytokines, including IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, transforming growth factor beta (TGF-beta), low-molecular-weight B-cell growth factor (BCGF), and interferon-gamma (IFN-gamma), did not induce IgA1 and IgA2 production in fetal B cells or pre-B cells. These findings indicate that, in the presence of costimulators, VIP may induce IgA1 and IgA2 production by isotype switching. (C) 1995 by The American Society of Hematology.