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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Impaired primary immune response in type-1 diabetes: results from a controlled vaccination study.
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Impaired primary immune response in type-1 diabetes: results from a controlled vaccination study.

机译：1型糖尿病的原发性免疫反应受损：来自对照疫苗接种研究的结果。

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Patients with diabetes have an increased risk for infections, but information on their adoptive immunity is incomplete and contradictory. Twenty patients with diabetes type-1 and 20 patients with type-2 diabetes were vaccinated with T-cell-dependent primary protein antigens (hepatitis A viral antigen, HAV; diphtheria toxoid) and a T-cell-independent polysaccharide antigen (pneumococcal polysaccharide). In parallel, the proliferative response of CD4+ T-cells to the primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. Compared to healthy controls, type-1 diabetes patients mounted a significantly impaired primary antibody response to hepatitis A vaccine (median HAV antibody titer after the first vaccination, 53 IU/L in diabetic patients vs 212 IU/L in the controls, P = 0.017) and diphtheria toxoid (median serum antibodies after vaccination, patients, 0.94 IU/ml, controls, 6.38 IU/ml, P = 0.004), while the response to pneumococcal polysaccharide was normal. Type-2 diabetes patients had a comparable metabolic dysregulation but showed a normal antibody response following vaccination, demonstrating that the effect was not due to hyperglycemia. Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. In addition, the proliferative response of CD4+ T-cells derived from type-1 diabetes patients to KLH and SWM was significantly reduced (P < or = 0.01). FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. An association of low HAV antibody response with HLA-DR3,4 expression in the patients was shown. Our results indicate that the primary antibody response to T-cell dependent antigens as well as the T-cell response to primary protein antigens is reduced in type-1 diabetes patients and that additional booster immunization can overcome the defect.
机译：糖尿病患者感染的风险增加，但是关于过继免疫的信息并不完整且相互矛盾。为20例1型糖尿病患者和20例2型糖尿病患者接种了T细胞依赖性初级蛋白抗原（甲型肝炎病毒抗原，HAV;白喉类毒素）和非T细胞依赖性多糖抗原（肺炎球菌多糖） 。平行地，使用单核细胞来源的树突状细胞（MDDC）作为抗原呈递细胞，在体外测量了CD4 + T细胞对主要蛋白抗原匙孔血蓝蛋白（KLH）和抹香鲸肌红蛋白（SWM）的增殖反应。与健康对照相比，1型糖尿病患者对甲型肝炎疫苗的一抗显着减弱（初次接种后HAV抗体滴度中位数，糖尿病患者为53 IU / L，对照组为212 IU / L，P = 0.017） ）和白喉类毒素（接种后中位血清抗体，患者，0.94 IU / ml，对照，6.38 IU / ml，P = 0.004），而对肺炎球菌多糖的反应正常。 2型糖尿病患者具有类似的代谢失调，但在接种疫苗后显示正常的抗体反应，表明该作用并非由于高血糖引起的。抗原诱导的干扰素-γ和白介素13释放在1型糖尿病患者中减少，将损伤定位在抗原呈递细胞-T细胞相互作用的水平。此外，源自1型糖尿病患者的CD4 + T细胞对KLH和SWM的增殖反应显着降低（P <或= 0.01）。在MDDC上对CD80（B7.1），CD86（B7.2）和HLA-DR表达的FACS分析无法证明在1型和2型糖尿病患者与健康对照者之间这些分子的表达有显着差异。显示了患者中低HAV抗体应答与HLA-DR3,4表达的关联。我们的结果表明，在1型糖尿病患者中，对T细胞依赖性抗原的初级抗体应答以及对初级蛋白抗原的T细胞应答均降低，并且额外的加强免疫可以克服该缺陷。

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