哮喘联盟

    背景：已有研究检测非过敏性哮喘患者气道上皮细胞蛋白的IgG自身抗体。
    目的和方法：为评价这些自身抗体功能上的重要性，我们采用来源于非过敏性哮喘患者的纯化的IgG抗体，通过微量细胞毒性分析，在气道上皮细胞（A549）中评价IgG 抗体诱导的细胞毒性作用。
    结果：9名非过敏性哮喘患者IgG 抗体诱导的细胞毒性（以细胞溶解百分数表示）（30.6±7.3%; p < 0.05）显著高于8名健康对照（均值±标准差：13.9±5.1%）和9名过敏性哮喘患者（20.3 ±10.4%），。此外，将非过敏性哮喘患者来源的IgG 抗体与重组人气道上皮细胞自身抗原（细胞角蛋白18或alpha-烯醇酶蛋白）预先孵育后，IgG 抗体诱导的细胞毒性作用被明显抑制（p < 0.05）。
    结论：这些结果表明，非过敏性哮喘的发病过程中IgG自身抗体参与诱导了气道上皮的细胞毒性作用。

（刘国梁 审校）
 Kwon B, et al. J Clin Immunol. 2009 Feb 13. [Epub ahead of print].

Increased IgG Antibody-Induced Cytotoxicity Against Airway Epithelial Cells in Patients with Nonallergic Asthma.

BACKGROUND: IgG autoantibodies to airway epithelial cell proteins have been detected in patients with nonallergic asthma.
OBJECTIVE AND METHODS: To evaluate the functional significance of these autoantibodies, we examined the presence of IgG antibody-induced cytotoxicity against airway epithelial cells (A549) by the microcytotoxicity assay using IgG antibodies purified from patients with nonallergic asthma.
RESULTS: IgG antibody-induced cytotoxicity (expressed as percent cell lysis) was significantly increased in nine patients with nonallergic asthma (mean +/- standard deviation; 30.6 +/- 7.3%) as compared with eight healthy controls (13.9 +/- 5.1%) and nine patients with allergic asthma (20.3 +/- 10.4%; p < 0.05). In addition, IgG antibody-induced cytotoxicity was significantly inhibited when IgG antibodies from patients with nonallergic asthma were pre-incubated with recombinant human airway epithelial cell autoantigens (cytokeratin 18 or alpha-enolase proteins; p < 0.05).
CONCLUSION: These results suggest a possible involvement of IgG autoantibody-induced cytotoxicity against airway epithelial cells in the pathogenesis of nonallergic asthma.