Immunoallergology Unit, Department of Medicine and Geriatrics, Careggi University Hospital, Florence, Italy.
Centre for Research, Transfer and High Education DENOTHE, Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Sci Rep. 2021 Jun 15;11(1):12558. doi: 10.1038/s41598-021-91851-7.
Biologic agents (BA) are able to induce an adaptive immune response in a proportion of exposed patients with the onset of anti-drug antibodies (ADA), which are usually responsible for hypersensitivity reactions (HR). Drug desensitization (DD) for BA allows transient clinical tolerance to the drug in reactive patients. The paper aimed to analyse the modification of drug-specific immune responses along DD in two patients with previous ADA-mediated HR (anaphylaxis) to rituximab and tocilizumab. The in vivo and in vitro assays of humoral and cellular response to drugs were carried out in a longitudinal manner throughout the DD cycles. We observed a progressive decrease of the pre-procedure ADA titer with negativization during the DD cycles in both patients. The monitoring of the drug-specific effector cell response showed the decrease in the BA-induced proliferation, while T cell response to unrelated antigens resulted unmodified along the DD cycles. Lastly, the increase of circulating drug-specific Treg cells mainly producing IL-35 were shown during the DD treatment. This study provides evidence that DD treatment to two BA inhibits humoral and cellular anti-drug response by increasing regulatory T cells and cytokines in an antigen-restricted manner. These modifications could contribute to the safety of the procedure.
生物制剂 (BA) 能够在一部分接触到药物的患者中诱导适应性免疫反应,从而产生抗药物抗体 (ADA),而这些抗体通常是导致过敏反应 (HR) 的原因。BA 的药物脱敏 (DD) 可使有反应性的患者暂时对药物产生临床耐受。本文旨在分析两例因抗 rituximab 和 tocilizumab 抗体导致 HR(过敏反应)而发生 ADA 介导的 HR 的患者在 DD 过程中对药物特异性免疫反应的改变。在 DD 周期内,我们通过纵向检测药物特异性体液和细胞反应,对这两例患者进行了体内和体外的检测。我们观察到,在两例患者的 DD 周期中,ADA 滴度逐渐降低,并且在治疗过程中逐渐转为阴性。同时,BA 诱导的增殖反应也逐渐降低,但 T 细胞对无关抗原的反应在 DD 周期内并未改变。最后,我们还观察到循环中药物特异性 Treg 细胞(主要产生 IL-35)的增加。本研究表明,DD 治疗可抑制两种 BA 的体液和细胞抗药物反应,其机制可能与增加调节性 T 细胞和细胞因子的表达有关,且这种调节具有抗原特异性。这些变化可能有助于提高该治疗方案的安全性。