Department of Dermatology, Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan.
Department of Pharmacotherapy, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Front Immunol. 2022 Jun 29;13:883605. doi: 10.3389/fimmu.2022.883605. eCollection 2022.
Sweat aggravates atopic dermatitis (AD). In patients with AD, type-I hypersensitivity to sweat may be shown by histamine release from patients' basophils in response to the semi-purified sweat antigen (QR), and the presence of specific immunoglobulin E (IgE) binding to MGL_1304, the component of QR. However, there has been no information on the immunological changes of type-I hypersensitivity to the sweat antigen in patients with well-controlled AD using topical corticosteroids (TCSs) and/or biologics as treatments.
Histamine-releasing tests using patients' basophils and QR and the detection of serum IgE against MGL_1304 and mite allergen Der f 1 were performed in patients with AD who were well controlled by topical TCS with/without dupilumab for 53-96 weeks.
In total, 14 patients were enrolled. Seven patients received TCS therapy alone (TCS group), and seven patients received TCS with dupilumab therapy (dupilumab group). In all participants, the level of specific IgE against MGL_1304 decreased after treatments, but histamine release from basophils in response to QR did not show a statistically significant reduction; rather, it increased. In the dupilumab group, all changes in histamine release induced by QR (increase), the IgE level against MGL_1304 (decrease), and that against Der f 1 (decrease) were statistically significant, whereas the TCS group showed no significant change in any of them.
The well-controlled condition for 53-96 weeks resulted in no reduction of the hyperreactivity of basophils against in patients with AD, even with the treatment with dupilumab. This study suggests persistent basophil hyperreactivity to sweat antigen over a year or longer.
汗液会加重特应性皮炎（AD）。在 AD 患者中，患者的嗜碱性粒细胞对 QR（半纯化的汗液抗原）中的半胱氨酸蛋白酶抑制剂 G1 （MGL_1304）的特异性 IgE 结合可能显示出对汗液的 I 型超敏反应。然而，对于使用局部皮质类固醇（TCS）和/或生物制剂治疗的 AD 患者，汗液抗原的 I 型超敏反应的免疫变化尚无信息。
对经过 53-96 周局部 TCS 联合/不联合度普利尤单抗治疗控制良好的 AD 患者进行了患者嗜碱性粒细胞 QR 组胺释放试验和血清 IgE 检测 against MGL_1304 和尘螨过敏原 Der f 1。
共纳入 14 例患者。7 例患者单独接受 TCS 治疗（TCS 组），7 例患者接受 TCS 联合度普利尤单抗治疗（度普利尤单抗组）。在所有参与者中，针对 MGL_1304 的特异性 IgE 水平在治疗后降低，但 QR 刺激嗜碱性粒细胞释放组胺没有显示出统计学意义的降低，反而增加了。在度普利尤单抗组中，QR 诱导的组胺释放的所有变化（增加）、针对 MGL_1304 的 IgE 水平（降低）和针对 Der f 1 的 IgE 水平（降低）均具有统计学意义，而 TCS 组则没有显示出任何变化。
53-96 周的良好控制条件并没有降低 AD 患者嗜碱性粒细胞对汗液抗原的高反应性，即使使用度普利尤单抗治疗也是如此。这项研究表明，AD 患者对汗液抗原的嗜碱性粒细胞高反应性可能持续一年或更长时间。
