Nakama T
Department of Dermatology, Kurume University School of Medicine, Japan.
Kurume Med J. 1995;42(2):95-106. doi: 10.2739/kurumemedj.42.95.
This study demonstrated not only the presence of house dust mite antigen (HDM)-specific IgE and IgG antibodies in the sera of 27 patients with atopic dermatitis (AD), but also considerably increased levels of serum eosinophil cationic protein (ECP) and uniformly nadir levels of plasma ECP, which provides evidence for ECP release from eosinophils in vitro. Besides blood eosinophilia, AD patients had an increased number of CD32+ eosinophils and EG2+ "activated" eosinophils; both of which, especially the latter, were significantly correlated with elevated levels of serum ECP. AD-source eosinophils had enhanced sensitivity for IgG-immune complexes corresponding to their increased expression of CD32, whereas neither HDM alone nor IgE/HDM-immune complex induced eosinophil activation. There were no gamma globulin-bearing cells in AD-source eosinophils, indicating that serum ECP levels may be dependent on EG2+ eosinophil numbers rather than the state of CD32-mediated eosinophil degranulation, as shown in vitro. Since HDM can cause an eczematous skin reaction accompanying the eosinophil accumulation and degranulation in sensitized AD, increased numbers of both CD32+ and EG2+ eosinophils according to the extent of AD severity indicates that these eosinophil in vivo generations and their subsequent functioning in the lesional skin may be regulated through HDM-initiated dermatitis events, and then, may form a vicious circle as the AD lesions spread.
本研究不仅证明了27例特应性皮炎(AD)患者血清中存在屋尘螨抗原(HDM)特异性IgE和IgG抗体,还发现血清嗜酸性粒细胞阳离子蛋白(ECP)水平显著升高,血浆ECP水平均处于最低点,这为体外嗜酸性粒细胞释放ECP提供了证据。除了血液嗜酸性粒细胞增多外,AD患者CD32 +嗜酸性粒细胞和EG2 +“活化”嗜酸性粒细胞数量增加;这两者,尤其是后者,与血清ECP水平升高显著相关。AD来源的嗜酸性粒细胞对IgG免疫复合物的敏感性增强,这与其CD32表达增加相对应,而单独的HDM或IgE / HDM免疫复合物均未诱导嗜酸性粒细胞活化。AD来源的嗜酸性粒细胞中没有携带γ球蛋白的细胞,这表明血清ECP水平可能取决于EG2 +嗜酸性粒细胞的数量,而不是如体外所示的CD32介导的嗜酸性粒细胞脱颗粒状态。由于HDM可在致敏的AD中引起伴有嗜酸性粒细胞积聚和脱颗粒的湿疹样皮肤反应,根据AD严重程度增加的CD32 +和EG2 +嗜酸性粒细胞数量表明,这些嗜酸性粒细胞在体内的生成及其在皮损中的后续功能可能通过HDM引发的皮炎事件来调节,然后,随着AD皮损的扩散可能形成恶性循环。