T Cell-Independent Regulation of IgE Antibody Production Induced by Surface-Linked Liposomal Antigen

T Cell-Independent Regulation of IgE Antibody Production Induced by Surface-Linked Liposomal Antigen
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表面连接脂质体抗原诱导的 T 细胞独立调节 IgE 抗体产生

DOI:
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发表时间:
2002
影响因子:
4.4
通讯作者:
T. Uchida
T. Uchida
中科院分区:
医学2区
文献类型:
--
作者:
M. Taneichi;S. Naito;H. Kato;Yuriko Tanaka;M. Mori;Y. Nakano;H. Yamamura;H. Ishida;K. Komuro;T. Uchida

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控制IgE抗体的产生对于预防IgE相关疾病是重要的。然而,在现有的信息相反的诱导IgE的生产,很少有人知道这种同种型的生产的调节,除了有据可查的机制,涉及T细胞亚群和它们的细胞因子产品。在这项研究中,我们证明了一种替代的方法来干扰IgE的产生,独立的T细胞的活性,这是在调查过程中发现的,旨在澄清IgE选择性无反应性诱导的表面偶联脂质体抗原的机制。用OVA-脂质体缀合物免疫小鼠诱导IgE选择性无反应性,而没有明显的Th 1极化。IL-12、IL-10和CD 8(+)T细胞均不参与调节。此外,OVA脂质体免疫小鼠的CD 4(+)T细胞能诱导明矾吸附的OVA免疫裸鼠产生Ag特异性IgE。相反,用OVA-脂质体免疫受体小鼠不诱导抗-OVA IgE产生,即使当转移用明矾吸附的OVA免疫的小鼠的CD 4(+)T细胞时。在二次免疫应答中,OVA-脂质体增强了抗OVA IgG Ab的产生,但它没有增强持续的IgE产生,这表明脂质体Ag诱导的IgE选择性无反应性涉及对IgE的直接影响,但不是体内IgG转换。这些结果表明,存在一种替代机制,不涉及T细胞在IgE合成的调节。
Control of IgE Ab production is important for the prevention of IgE-related diseases. However, in contrast to the existing information on the induction of IgE production, little is known about the regulation of the production of this isotype, with the exception of the well-documented mechanism involving T cell subsets and their cytokine products. In this study, we demonstrate an alternative approach to interfere with the production of IgE, independent of the activity of T cells, which was discovered during the course of an investigation intended to clarify the mechanism of IgE-selective unresponsiveness induced by surface-coupled liposomal Ags. Immunization of mice with OVA-liposome conjugates induced IgE-selective unresponsiveness without apparent Th1 polarization. Neither IL-12, IL-10, nor CD8(+) T cells participated in the regulation. Furthermore, CD4(+) T cells of mice immunized with OVA-liposome were capable of inducing Ag-specific IgE synthesis in athymic nude mice immunized with alum-adsorbed OVA. In contrast, immunization of the recipient mice with OVA-liposome did not induce anti-OVA IgE production, even when CD4(+) T cells of mice immunized with alum-adsorbed OVA were transferred. In the secondary immune response, OVA-liposome enhanced anti-OVA IgG Ab production, but it did not enhance ongoing IgE production, suggesting that the IgE-selective unresponsiveness induced by the liposomal Ag involved direct effects on IgE, but not IgG switching in vivo. These results suggest the existence of an alternative mechanism not involving T cells in the regulation of IgE synthesis.