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MECHANISM OF ALLERGIC SENSITIZATION DURING INFANCY

婴儿期过敏致敏机制

基本信息

批准号：
09670792
负责人：
YACHIE Akihiro
金额：
$ 1.92万
依托单位：
KANAZAWA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

项目摘要

It is known that environmental factors, in addition to atopic diathesis play important roles in the development of allergic diseases during infancy and early childhood. In particular, massive allergen exposure during early infancy may lead to development of variable allergic symptoms by accelerating pre-existing allergic inflammation in susceptible individuals. The present research was undertaken to answer following questions.1) Age-dependent changes in serum IgE concentration and FcEPSILONel expression on circulating basophils.2) Mechanism of IgE production by neonatal B cells. Augmentation of IgE synthesis through CD7O/CD27.3) Pathophysiology of severe atopic dermatitis and primary immunodeficiency disorders.Serum IgE concentration increased age-dependently in allergic children. FcepsilonRI expression on peripheral blood basophils increased rapidly after birth and it bound 1gB efficiently. 1gB itself enhanced FcepsilonRI expression and 1gB binding on basophil surface. The enhancement of surface receptor expression was dependent on de novo protein sysnthesis together with the stabilization of the receptor proteins on the membrane by direct 1gE binding.Furthermore, IgE synthesis by neonatal or naive B cells was significantly enhanced by addition of CD7O-transfected cells into the culture. These effect was not seen when CD27 negative B cells were cultured. These findings, together with our previous reports on IgG production by neonatal BETA cells, disclosed the roles played by TAU cell derived cytokines and the surface ligands in the differentiation of neonatal BETA cells into plasma cells.Finally, the detailed pathophysiological examination of various immunodeficiency disorders with allergic manifestation presented several significant roles played by immune system in regulating allergic inflammation.

众所周知，环境因素，除了特应性素质发挥重要作用的过敏性疾病的发展，在婴儿期和幼儿期。特别是，婴儿早期大量接触过敏原可能会加速易感个体先前存在的过敏性炎症，从而导致各种过敏症状的发展。本研究旨在回答以下问题：1）血清IgE浓度和循环嗜碱性粒细胞上FcEPSILONel表达的依赖性变化; 2）新生儿B细胞产生IgE的机制。通过CD 7 O/CD 27增加IgE合成。3）严重特应性皮炎和原发性免疫缺陷疾病的病理生理学。过敏儿童血清IgE浓度随年龄增加而增加。FcepsilonRI在出生后外周血嗜碱性粒细胞上的表达迅速增加，并有效地结合1gB。1gB自身增强FcepsilonRI表达和1gB在嗜碱性粒细胞表面的结合。表面受体表达的增强依赖于从头蛋白质合成以及通过直接结合IgE稳定膜上的受体蛋白。此外，新生或幼稚B细胞的IgE合成通过向培养物中加入CD 7 O转染的细胞而显著增强。当培养CD 27阴性B细胞时，未观察到这些作用。这些发现与我们以前关于新生儿BETA细胞产生IgG的报道一起，揭示了TAU细胞源性细胞因子和表面配体在新生儿BETA细胞向浆细胞分化中所起的作用。最后，对各种免疫缺陷疾病伴过敏性表现的详细病理生理学检查提出了免疫系统在调节过敏性炎症中所起的几个重要作用。