Cross-Linking Surface Ig Delays CD40 Ligand- and IL-4-Induced B Cell Ig Class Switching and Reveals Evidence for Independent Regulation of B Cell Proliferation and Differentiation1

Cross-Linking Surface Ig Delays CD40 Ligand- and IL-4-Induced B Cell Ig Class Switching and Reveals Evidence for Independent Regulation of B Cell Proliferation and Differentiation1
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交联表面 Ig 延迟 CD40 配体和 IL-4 诱导的 B 细胞 Ig 类别转换,并揭示 B 细胞增殖和分化独立调节的证据1

DOI:
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发表时间:
2002
影响因子:
4.4
通讯作者:
P. Hodgkin
P. Hodgkin
中科院分区:
医学2区
文献类型:
--
作者:
J. Rush;J. Hasbold;P. Hodgkin

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T细胞以可诱导的膜结合分子和分泌细胞因子的形式提供激活信号,刺激B细胞分裂和分化。在没有任何形式的Ag刺激的情况下,在体外提供这些信号再现了T-B协同的许多后果。虽然显然不是强制性的,但Ag信号似乎在B细胞反应的许多方面发挥重要的调节作用。为了直接检测Ag信号的作用,在rCD40配体存在的情况下,在存在或不存在不同的抗ig单抗的情况下,用IL-4或不含IL-4刺激幼稚B细胞。抗igg单抗对B细胞分裂率有不同的影响,从增强到无影响到抑制。相反,所有抗igg单克隆抗体检测抑制分裂连锁同型转换到IgG1和IgE。因此,B细胞Ag受体配体可以独立地改变B细胞扩增和类转换的速率。抗Ig试剂改变类转换的能力表明,在T细胞依赖的针对不同物理结构Ags的体液免疫反应中,B细胞Ag受体可能在Ig同种型的选择中发挥重要作用。
T cells stimulate B cells to divide and differentiate by providing activating signals in the form of inducible membrane-bound molecules and secreted cytokines. Provision of these signals in vitro reproduces many of the consequences of T-B collaboration in the absence of any form of Ag stimulation. Although clearly not obligatory, Ag signals appear to play an important regulatory role in numerous aspects of the B cell response. To examine directly the effect of an Ag signal, naive B cells were stimulated in the presence of rCD40 ligand, with or without IL-4 in the presence or absence of different anti-Ig mAbs. Anti-Ig mAbs exerted variable effects on the B cell division rate, from enhancement to no effect to inhibition. In contrast, all anti-Ig mAbs tested inhibited division-linked isotype switching to IgG1 and IgE. Thus, B cell Ag receptor ligands could modify the rates of B cell expansion and class switching independently. The ability of anti-Ig reagents to modify class switching suggests the B cell Ag receptor may play an important role in the selection of Ig isotypes during T cell-dependent humoral immune responses to Ags of different physical structure.
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