首页> 外文OA文献 >Influenza virus vaccination induces interleukin-12/23 receptor beta 1 (IL-12/23R beta 1)-independent production of gamma interferon (IFN-gamma) and humoral immunity in patients with genetic deficiencies in IL-12/23R beta 1 or IFN-gamma receptor I
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Influenza virus vaccination induces interleukin-12/23 receptor beta 1 (IL-12/23R beta 1)-independent production of gamma interferon (IFN-gamma) and humoral immunity in patients with genetic deficiencies in IL-12/23R beta 1 or IFN-gamma receptor I

机译:患有IL-12 / 23R beta 1或IFN基因缺陷的患者中的流感病毒疫苗诱导白介素12/23受体beta 1(IL-12 / 23R beta 1)依赖性γ干扰素(IFN-γ)产生和体液免疫-γ受体I

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摘要

To investigate whether protective immune responses can be induced in the absence of normal interleukin12/23/gamma interferon (IL-12/23/IFN-gamma) axis signaling, we vaccinated with the seasonal influenza virus subunit vaccine two patients with complete IL-12/23 receptor beta 1 (IL-12/23R beta 1) deficiencies, two patients with partial IFN-gamma receptor I (pIFN-gamma RI) deficiencies, and five healthy controls. Blood samples were analyzed before, 7 days after, and 28 days after vaccination. In most cases, antibody titers reached protective levels. Moreover, although T-cell responses in patients were lower than those observed in controls, significant influenza virus-specific T-cell proliferation, IFN-gamma production, and numbers of IFN-gamma-producing cells were found in all patients 7 days after the vaccination. Interestingly, influenza virus-specific IFN-gamma responses were IL-12/23 independent, in striking contrast to mycobacterium-induced IFN-gamma production. In conclusion, influenza virus vaccination induces IL-12/23-independent IFN-gamma production by T cells and can result in sufficient humoral protection in both IL-12/23R beta 1- and pIFN-gamma RI-deficient individuals
机译:为了研究在缺乏正常白介素12/23 /γ干扰素(IL-12 / 23 /IFN-γ)轴信号的情况下是否可以诱导保护性免疫应答,我们给季节性流感病毒亚单位疫苗接种了两名完全IL-12的患者/ 23受体beta 1(IL-12 / 23R beta 1)缺陷,两名患有部分IFN-γ受体I(pIFN-γRI)缺陷的患者和五个健康对照组。在接种前,接种后7天和接种后28天分析血样。在大多数情况下,抗体滴度达到保护水平。此外,尽管患者的T细胞反应低于对照组,但在感染后7天,所有患者均发现明显的流感病毒特异性T细胞增殖,IFN-γ产生和IFN-γ产生细胞的数量。疫苗接种。有趣的是,流感病毒特异性IFN-γ反应与IL-12 / 23无关,这与分枝杆菌诱导的IFN-γ产生形成鲜明对比。总之,流感疫苗接种可诱导T细胞产生IL-12 / 23不依赖的IFN-γ,并可以在IL-12 / 23R beta 1-和pIFN-γRI缺陷个体中获得足够的体液保护

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