Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, Medical University of Vienna, Austria.
J Dtsch Dermatol Ges. 2010 Dec;8(12):990-8. doi: 10.1111/j.1610-0387.2010.07497.x.
Our understanding of the pathogenic role of IgE in atopic dermatitis is incomplete. We asked whether blocking free IgE would alter the course of the disease.
We administered either omalizumab, a humanized monoclonal mouse antibody against IgE, or placebo subcutaneously for 16 weeks to 20 atopic dermatitis patients and measured immunological and clinical disease parameters.
Omalizumab (I) reduced free serum IgE, (II) lowered surface IgE and FcɛRI expression on different peripheral blood mononuclear cells, (III) reduced the saturation of FcɛRI with IgE, (IV) increased the number of free FcɛRI and (V) lowered the number of IgE+, but not of FcɛRI+ cells in skin. The in vivo relevance of these results is evidenced by the increase in the threshold allergen concentration required to give a type I hypersensitivity reaction in the titrated skin test. While not significantly altering the clinical disease parameters, omalizumab treatment led to an improvement of the atopy patch test results in single patients, i.e. an eczematous reaction upon epicutaneous allergen challenge.
The interference with immediate and delayed type skin tests may imply that a therapeutic benefit of omalizumab treatment, if present at all, would be seen in patients with acute rather than chronic forms of the disease.
我们对 IgE 在特应性皮炎发病机制中的作用的了解并不完全。我们想知道是否阻断游离 IgE 会改变疾病的进程。
我们对 20 例特应性皮炎患者进行皮下注射奥马珠单抗(一种针对 IgE 的人源化单克隆鼠抗体)或安慰剂治疗 16 周,并测量免疫和临床疾病参数。
奥马珠单抗(I)降低了游离血清 IgE,(II)降低了不同外周血单个核细胞表面 IgE 和 FcɛRI 的表达,(III)降低了 FcɛRI 与 IgE 的饱和度,(IV)增加了游离 FcɛRI 的数量,(V)降低了皮肤中 IgE+但不降低 FcɛRI+细胞的数量。这些结果的体内相关性由皮试中过敏原浓度阈值的增加所证实,该阈值可引发 I 型超敏反应。奥马珠单抗治疗虽然没有显著改变临床疾病参数,但在个别患者中导致特应性皮炎斑贴试验结果的改善,即经皮过敏原挑战时出现湿疹反应。
对即刻和迟发型皮肤试验的干扰意味着奥马珠单抗治疗的治疗益处,如果存在的话,将见于急性而非慢性疾病患者。