Activation of influenza virus-specific CD4+ and CD8+ T cells:: a new role for plasmacytoid denchitic cells in adaptive immunity

Activation of influenza virus-specific CD4+ and CD8+ T cells:: a new role for plasmacytoid denchitic cells in adaptive immunity
复制标题

DOI:
10.1182/blood-2002-10-3063
复制
发表时间:
2003-05-01
期刊:
影响因子:
20.3
通讯作者:
Bhardwaj, N
Bhardwaj, N
中科院分区:
医学1区
文献类型:
--
作者:
Fonteneau, JF;Gilliet, M;Bhardwaj, N

文献摘要

被引文献

相似文献

浆细胞样树突状细胞 (pDC) 在接触包膜病毒时产生 I 型干扰素 (IFN),从而促进先天抗病毒免疫反应。然而,它们在适应性免疫反应(例如抗病毒 T 细胞反应的启动)中的作用尚不清楚。在这项研究中,我们检查了血液 pDC 和流感病毒之间的相互作用,特别关注 pDC 激活流感特异性 T 细胞的能力。将 pDC 与最有效的抗原呈递细胞 (APC) CD11c(+) DC 进行比较,以确定它们激活 T 细胞反应的能力。我们发现,与CD11c(+) DCs一样,pDCs在暴露于流感病毒后成熟,表达CCR7并产生促炎趋化因子,但不同之处在于它们产生I型IFN并且对感染的细胞病变效应具有抵抗力。暴露于流感病毒后,两种DC类型在扩增抗流感病毒细胞毒性T淋巴细胞(CTL)和辅助性T I(THII)CD4(+)T细胞方面表现出相同的效率。我们的结果查明了 pDC 在诱导抗病毒 T 细胞反应中的新作用,并表明这些 DC 在针对病毒的适应性免疫反应中发挥着重要作用。 (C) 2003 年,美国血液学会。
Plasmacytoid dendritic cells (pDCs) contribute to innate antiviral immune responses by producing type I interferons (IFNs) upon exposure to enveloped viruses. However, their role in adaptive immune responses, such as the initiation of antiviral T-cell responses, is not known. In this study, we examined interactions between blood pDCs and influenza virus with special attention to the capacity of pDCs to activate influenza-specific T cells. pDCs were compared with CD11c(+) DCs, the most potent antigen-presenting cells (APCs), for their capacity to activate T-cell responses. We found that like CD11c(+) DCs, pDCs mature following exposure to influenza virus, express CCR7, and produce proinflammatory chemokines, but differ in that they produce type I IFN and are resistant to the cytopathic effect of the infection. After influenza virus exposure, both DC types exhibited an equivalent efficiency to expand anti-influenza virus cytotoxic T lymphocytes (CTLs) and T helper I (THII) CD4(+) T cells. Our results pinpoint a new role of pDCs in the induction of antiviral T-cell responses and suggest that these DCs play a prominent role in the adaptive immune response against viruses. (C) 2003 by The American Society of Hematology.