Allardyce R A, Bienenstock J
Bull World Health Organ. 1984;62(1):7-25.
This article briefly describes the network of immunity involving selected humoral and cellular elements shared between mucosal surfaces that are both exposed to and remote from antigen challenge. The mechanisms promoting the production, concentration, and secretion of specific antibody isotypes, as well as the migration and localization of various lymphoid cell populations, have been discussed with regard to host mucosal protection against pathogenic agents and other potentially harmful macromolecules.Although certain aspects of the mucosal immune system may be viewed as separate from the systemic immune system, they are not exclusively so. We have drawn attention to their interactions with systemic immune reactants and other, nonimmunological, cellular and humoral constituents of mucosal surfaces and tissues such as the liver. At another level of interaction we have considered the teleological translation of host defence and immunoregulation from one generation to the next through the medium of colostrum and breast milk.The manipulation of the mucosal immune system in order to enhance host resistance, modulate autoimmune and allergic systemic reactivity, or even modify fertility holds great promise. Achievement of these goals depends on gaining further insight into the mechanisms that contribute to mucosal immunity and their interactions with the systemic immune system. Much of our current knowledge is based upon experimental animal models or human populations living in relative prosperity. However, the results of oral vaccination, for example, are known to differ considerably in populations that suffer from parasitic infestations, lack adequate nutrition, and are very old or very young. We have chosen to focus attention on these groups because they constitute a large proportion of the world's population and because mucosal infections are a common cause of illness and death among them.Lastly, the recent discovery that immune deficiencies due to insufficient dietary zinc may extend to subsequent generations of optimally nourished offspring calls for a re-evaluation of immunization protocols in malnourished populations, and of our current understanding of disease inheritance and susceptibility.
本文简要描述了免疫网络,该网络涉及黏膜表面之间共享的特定体液和细胞成分,这些黏膜表面既暴露于抗原挑战又远离抗原挑战。关于宿主黏膜针对病原体和其他潜在有害大分子的保护,已经讨论了促进特定抗体同种型产生、浓缩和分泌的机制,以及各种淋巴细胞群体的迁移和定位。尽管黏膜免疫系统的某些方面可能被视为与全身免疫系统分开,但并非完全如此。我们已提请注意它们与全身免疫反应物以及黏膜表面和组织(如肝脏)的其他非免疫细胞和体液成分的相互作用。在另一个相互作用层面,我们考虑了通过初乳和母乳将宿主防御和免疫调节从一代传递到下一代的目的论转化。
操纵黏膜免疫系统以增强宿主抵抗力、调节自身免疫和过敏性全身反应性,甚至改变生育能力,具有很大的前景。实现这些目标取决于进一步深入了解促成黏膜免疫的机制及其与全身免疫系统的相互作用。我们目前的许多知识基于实验动物模型或生活相对富足的人群。然而,例如,已知口服疫苗的结果在遭受寄生虫感染、缺乏足够营养、年龄很大或很小的人群中差异很大。我们选择关注这些群体,是因为他们占世界人口的很大比例,而且黏膜感染是他们患病和死亡的常见原因。
最后,最近发现由于饮食锌不足导致的免疫缺陷可能会延续到营养状况最佳的后代的后续几代,这就需要重新评估营养不良人群的免疫接种方案,以及我们目前对疾病遗传和易感性的理解。