Thrower S L, James L, Hall W, Green K M, Arif S, Allen J S, Van-Krinks C, Lozanoska-Ochser B, Marquesini L, Brown S, Wong F S, Dayan C M, Peakman M
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, UK.
Clin Exp Immunol. 2009 Feb;155(2):156-65. doi: 10.1111/j.1365-2249.2008.03814.x. Epub 2008 Nov 20.
Immunotherapeutic strategies under consideration for type 1 diabetes include modification of the autoimmune response through antigen-specific routes. Administration of short peptides representing T cell epitopes targeted by patients with the disease represents one approach. This study evaluated safety and mechanistic outcomes during first-in-man intradermal administration of a human leucocyte antigen-DR4 (HLA-DR4)-restricted peptide epitope of proinsulin (C19-A3). This randomized, open-label study assessed two major theoretical risks of peptide immunotherapy, namely induction of allergic hypersensitivity and exacerbation of the proinflammatory autoimmune response, using clinical assessment and mechanistic assays in vitro. Patients with long-standing type 1 diabetes and HLA-DRB1*0401 genotype received 30 microg (n = 18) or 300 microg (n = 18) of peptide in three equal doses at 0, 1 and 2 months or no intervention (n = 12). Proinsulin peptide immunotherapy in the dosing regimen used is well tolerated and free from risk of systemic hypersensitivity and induction/reactivation of proinsulin-specific, proinflammatory T cells. Peptide-specific T cells secreting the immune suppressive cytokine interleukin (IL)-10 were observed at month 3 in four of 18 patients in the low-dose group (versus one of 12 in the control group; P = not significant). Mean IL-10 response to peptide in the low-dose group increased between 0 and 3 months (P = 0.05 after stimulation with 5 microM peptide in vitro) and then declined to baseline levels between 3 and 6 months (P = 0.01 at 10 microM peptide in vitro). These studies pave the way for future investigations in new-onset patients designed to examine whether proinsulin peptide immunotherapy has beneficial effects on markers of T cell autoimmunity and preservation of beta cell mass.
正在考虑用于1型糖尿病的免疫治疗策略包括通过抗原特异性途径改变自身免疫反应。给予代表该疾病患者靶向的T细胞表位的短肽是一种方法。本研究评估了人胰岛素原(C19-A3)的人白细胞抗原-DR4(HLA-DR4)限制性肽表位首次皮内给药期间的安全性和机制结果。这项随机、开放标签研究使用临床评估和体外机制分析评估了肽免疫治疗的两个主要理论风险,即诱导过敏性超敏反应和促炎性自身免疫反应的加剧。患有长期1型糖尿病且HLA-DRB1*0401基因型的患者在0、1和2个月时接受三剂等量的30微克(n = 18)或300微克(n = 18)肽,或不进行干预(n = 12)。所用给药方案中的胰岛素原肽免疫治疗耐受性良好,无全身超敏反应风险,也不会诱导/重新激活胰岛素原特异性促炎性T细胞。低剂量组18名患者中有4名在第3个月观察到分泌免疫抑制细胞因子白细胞介素(IL)-10的肽特异性T细胞(对照组12名患者中有1名;P = 无显著性差异)。低剂量组对肽的平均IL-10反应在0至3个月之间增加(体外5 microM肽刺激后P = 0.05),然后在3至6个月之间降至基线水平(体外10 microM肽时P = 0.01)。这些研究为未来对新发患者的研究铺平了道路,旨在检查胰岛素原肽免疫治疗是否对T细胞自身免疫标志物和β细胞质量的保存有有益作用。