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IMMUNOLOGICAL AND GENETIC STUDY ON IgEFc RECEPTOR IN PATIENTS WITH ATOPIC BRONCHIAL ASTHMA

特应性支气管哮喘患者IgEFc受体的免疫学和遗传学研究

基本信息

批准号：
01480232
负责人：
KAWAKAMI Yoshikazu
金额：
$ 4.1万
依托单位：
HOKKAIDO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

项目摘要

We investigated the expression of low affinity receptor for IgE Fc portion (Fc epsilon R II), which plays a major roles in atopic bronchial asthma. An increase in the intensity of expression of Fc epsilon R II and the proportion of cells bearing thi13EA\ : s antigen was observed for peripheral B cells in atopic bronchial asthma. In contrast, no such heightened expression was observed for T cells both in peripheral blood and bronchoalveolar lavage fluid. Levels of soluble Fc epsilon R II) were not incr13EA\ : eased in patients' serum. Patients with pulmonary sarcoidosis, who had increased serum levels of interferon-gamma which competed with IL-4 in regulatory roles of Fc epsilon R II, did not show decreased serum Fc epsilon R II levels. Thus, these resul13EA\ : ts suggest that membrane-bound Fc epsilon R II (mFc epsilon R II) on B cell surface is more appropriate than sFc epsilon R II as a marker of type I allergic reaction.We next cultured peripheral blood B cells in vitro in the prese … More nce of IL-4 and examined the expression of mFc epsilon R II and production of sFc epsilon R II.No significant difference in these parameters was observed between normal subjects and pat13EA\ : ients with atopic bronchial asthma or pulmonary sarcoidosis. Accordingly, it seemed that the increased expression of Fc epsilon R II in fresh B cells was not due to inherent alterations in IL-4-responsiveness of atopic patients.To search for a locus of gene responsible for atopy defined as hightened state of lgE production, we examined linkage between atopy and locus 11q13, using restriction fragment length polymorphism (RFLP) of a marker DNA.No significant linkage was fo13EA\ : und for 58 members from 4 families which included a atopic patient as a proband, which sharply contradicted the previous report from Britain. Thus, our study failed to confirm the notion that a gene at locus 11q13 or near this locus determined atopy13EA\ : . However, the presence of one of 5 alleles detected by the same DNA probe was significantly associated with high serum IgE, thus suggesting that some gene at/near this locus was partially responsible for appearance of atopy. Less

我们研究了在特应性支气管哮喘中起主要作用的IgE Fc部分低亲和力受体（Fc epsilon R II）的表达。在特应性支气管哮喘患者外周血B细胞中，Fc epsilon Rⅱ表达强度升高，携带thi13EA\: s抗原的细胞比例增加。相比之下，外周血和支气管肺泡灌洗液中均未观察到T细胞表达升高。患者血清中可溶性Fc （Rⅱ）水平未升高或降低。肺结节病患者血清中干扰素- γ水平升高，与IL-4竞争Fc - epsilon R II的调节作用，但血清中Fc - epsilon R II水平并未下降。因此，这些结果表明，B细胞表面膜结合的Fc epsilon R II （mFc epsilon R II）比sFc epsilon R II更适合作为I型过敏反应的标志物。在IL-4浓度下体外培养外周血B细胞，检测mFc epsilon R II的表达和sFc epsilon R II的产生。这些参数在正常受试者和特应性支气管哮喘或肺结节病患者之间无显著差异。因此，新鲜B细胞中Fc epsilon R II表达的增加似乎不是由于特应性患者il -4反应性的固有改变。为了寻找与特异性相关的基因位点，我们利用标记DNA的限制性片段长度多态性（RFLP）研究了特异性与位点11q13之间的联系。来自4个家庭的58名成员，其中包括一名特应性反应患者作为先证者，没有发现明显的联系，这与之前英国的报告严重矛盾。因此，我们的研究未能证实11q13位点或该位点附近的基因决定了atopy13EA\：。然而，在同一DNA探针检测到的5个等位基因中，有一个的存在与高血清IgE显著相关，这表明该位点上或附近的某些基因对特应性的出现负有部分责任。少