低亲和力IgE受体与外源性支气管哮喘  

Low-affinity IgE Receptor and Exogenous Bronchial Asthma

作　　者：夏国光[1] 王丹琪[1] 赵树林[1] 陈慰峰[1] 

机构地区：[1]北京医科大学第四临床医学院积水潭医院呼吸内科,北京医科大学免疫教研组

出　　处：《心肺血管病杂志》1996年第3期172-174,共3页Journal of Cardiovascular and Pulmonary Diseases

摘　　要：本文对３０例外源性哮喘患者及３０例正常人的外周血单个核细胞（ＭＮＣ）低亲和力ＩｇＥ受体（即ＣＤ２３）表达、白细胞介素－４（ＩＬ－４）及血清ＩｇＥ水平进行测定。结果显示：发作组哮喘患者ＩｇＥ、ＩＬ－４、ＣＤ２３与缓解组及正常对照组之间有显著性差异（Ｐ＜０．０１）。且ＩｇＥ升高与ＣＤ２３呈正相关（ｒ＝０．８２７；Ｐ＜０．０１）。缓解组ＩｇＥ抗体、ＩＬ－４与正常对照组之间无显著性差异（Ｐ＞０．０５）；ＣＤ２３与正常对照组之间有显著性差异（Ｐ＜０．０ｌ）。以上结果表明了这一细胞因子的失衡与外源性哮喘的关系。Peripheral low-affinity IgE receptor(CD23),interleukin-4(IL-4),and Serum IgE level were measured in 30 patients with exogenous bronchial asthma and in 30 normal adults.The results showed that the levels of IgE,IL-4,and CD23 in patients with bronchial asthma at acute stage were significantly different from those in patients at remission stage and in the normal controls(P<0.01).The increase of IgE was positively related to CD23(r=0.827,P<0.01).The levels of IgE and IL-4 in patients with bronchial asthma at remission stage were not statistically different from those in the normal controls(P>0.05), while their CD23 differed significantly(P<0.01).Our study demonstrated that increased production of IgE antibody is the key factor in the onset of exogenous asthma.IL-4 activated B cells and thus promoted the expression of IgE receptor(CD23)on B cells, The increased CD23 expression could, in turn,enhance IgE synthesis in B cells induced by IL-4.The present study was undertaken to explore the relationship between the imbalance of cytokines and exogenous asthma.

关 键 词：哮喘 CD23 IGE抗体 IL-4 

分 类 号：R562.25[医药卫生—呼吸系统]