Ishizuka T, Okayama Y, Kobayashi H, Mori M
First Department of Internal Medicine, Gunma University, School of Medicine, Maebashi, Japan.
Inflammation. 1999 Feb;23(1):25-35. doi: 10.1023/a:1020235400073.
The cytokine interleukin (IL)-3 is important in the proliferation of eosinophils and basophils in the airway. We investigated IL-3 production by human lung mast cells as a possible mechanism of the airway inflammation constituting the late asthmatic response. Mast cells were purified using affinity magnetic selection with the monoclonal antibody YB5.B8 and then stimulated with anti-human IgE antibody. IL-3 release was detectable by enzyme-linked immunosorbent assay 8 h after anti-IgE stimulation. IL-3 release 24 h after anti-IgE stimulation was significantly greater than its controls. By reverse transcription-polymerase chain reaction, IL-3 mRNA was detected weakly 2 h after anti-IgE stimulation, peaking at 4 h and waning at 8 h. Immunocytochemistry to localize IL-3 demonstrated mast cell staining. These results suggest that mast cells release IL-3 in response to high-affinity IgE receptor.
细胞因子白细胞介素(IL)-3在气道嗜酸性粒细胞和嗜碱性粒细胞的增殖中起重要作用。我们研究了人肺肥大细胞产生IL-3的情况,将其作为构成迟发性哮喘反应的气道炎症的一种可能机制。使用单克隆抗体YB5.B8通过亲和磁选法纯化肥大细胞,然后用抗人IgE抗体进行刺激。抗IgE刺激8小时后,通过酶联免疫吸附测定法可检测到IL-3的释放。抗IgE刺激24小时后的IL-3释放量显著高于其对照。通过逆转录-聚合酶链反应,抗IgE刺激2小时后可微弱检测到IL-3 mRNA,4小时达到峰值,8小时后下降。用于定位IL-3的免疫细胞化学显示肥大细胞染色。这些结果表明,肥大细胞响应高亲和力IgE受体释放IL-3。