T dependent induction of an IgA and IgM anti-polysaccharide response.

T dependent induction of an IgA and IgM anti-polysaccharide response.
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IgA 和 IgM 抗多糖反应的 T 依赖性诱导。

DOI:
10.1007/978-1-4684-5344-7_18
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发表时间:
1987
影响因子:
--
通讯作者:
Murray,PD
Murray,PD
中科院分区:
医学4区
文献类型:
--
作者:
Kagnoff,MF;Murray,PD

文献摘要

被引文献

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肠粘膜是免疫系统与许多外来抗原和病原体之间相互作用的第一个部位(1)。与多糖抗原的主要相互作用发生在肠道中,并且对细菌多糖的免疫应答在粘膜表面的宿主防御中是重要的。新生儿和老年人感染包囊细菌的发病率和死亡率很高。关于抗多糖免疫如何在粘膜表面调节以及在老化过程中调节的变化的信息对于改变抗多糖免疫的策略和免疫程序的设计具有重要价值。对聚合多糖如葡聚糖或果聚糖的抗体应答的诱导和调节在几个方面不同于对蛋白质或与蛋白质偶联的多糖的诱导和调节(2-8)。例如,对细菌多糖的反应主要是IgM和伊加类,以及小鼠中的IgG 3亚类(2,9-12)。此类分子具有有限数量的抗原决定簇,并引发有限异质性的抗体(13,14)。多糖的B细胞前体可以在出生后几天检测到(15)。尽管如此,与蛋白质相比,体内免疫后,对多糖的抗体应答可能在个体发育中延迟(2,4,15,16)。在人类中也观察到抗多糖免疫的发病年龄延迟(17)。
The intestinal mucosa is the first site of interaction between the immune system and many foreign antigens and pathogens (1). Major interactions with polysaccharide antigens take place in the gut, and immune responses to bacterial polysaccharides are important in host defenses at mucosal surfaces. Morbidity and mortality from infections with encapsulated bacteria is high in neonates and the elderly. Information regarding how anti-polysaccharide immunity is regulated at mucosal surfaces and changes in that regulation during aging could be of substantial value for strategies to alter anti-polysaccharide immunity and for the design of immunization programs.The induction and regulation of antibody responses to polymeric polysaccharides like the dextrans or levans differs in several respects from that to proteins or polysaccharides coupled to proteins (2-8). For example, responses to bacterial polysaccharides are largely of the IgM and IgA class, and the IgG3 subclass in mice (2, 9-12). Such molecules have a limited number of antigenic determinants and elicit antibodies of restricted heterogeneity (13, 14). B cell precursors for polysaccharides can be detected a few days after birth (15). Nonetheless, compared to p~ oteins, antibody responses to polysaccharides may be delayed in ontogeny after in vivo immunization (2, 4, 15, 16). Delays in the age of onset of antipolysaccharide immunity are seen also in humans (17).