Interleukin-1-inhibitor activity induced by respiratory syncytial virus: abrogation of virus-specific and alternate human lymphocyte proliferative responses.
Interleukin-1-inhibitor activity induced by respiratory syncytial virus: abrogation of virus-specific and alternate human lymphocyte proliferative responses.
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DOI：
10.1093/infdis/163.1.71
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
A. Salkind;D. McCarthy;J. Nichols;F. Domurat;E. Walsh;N. Roberts
中科院分区：
文献类型：
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作者：
A. Salkind;D. McCarthy;J. Nichols;F. Domurat;E. Walsh;N. Roberts
研究表明，呼吸道合胞病毒（RSV）感染可诱导人单核白细胞（MNL）产生净白细胞介素-1（IL-1）抑制剂活性。在目前IL-1抑制剂作用的研究中，将RSV暴露的细胞与假暴露或暴露于灭活RSV或流感病毒（其诱导净IL-1活性并通常增强有效的同型免疫）的自体MNL进行了比较。MNL暴露于流感病毒或灭活RSV导致人类白细胞抗原-DR、IL-2受体和转铁蛋白受体的表达增加，并通过3天的细胞周期增加进展。相比之下，暴露于感染性RSV导致标志物表达降低和细胞周期停滞，同时响应于病毒或其他刺激的增殖消失。这些数据提出了这样的可能性：RSV感染复发的一个促成机制是由于净IL-1抑制剂活性而早期抑制病毒特异性淋巴细胞的克隆扩张。
Respiratory syncytial virus (RSV) infection has been shown to induce human mononuclear leukocyte (MNL) production of net interleukin-1 (IL-1)-inhibitor activity. In the current studies of IL-1-inhibitor effects, RSV-exposed cells were compared with autologous MNL that were sham-exposed or exposed to inactivated RSV or influenza virus (which induces net IL-1 activity and commonly elicits effective homotypic immunity). Exposure of MNL to influenza virus or inactivated RSV resulted in increased expression of human leukocyte antigen-DR, the IL-2 receptor, and the transferrin receptor and increased progression through the cell cycle by 3 days. In contrast, exposure to infectious RSV resulted in decreased marker expression and cell cycle arrest, with abrogation of proliferation in response to the virus or other stimuli. These data raise the possibility that a contributing mechanism for recurrence of RSV infection is early suppression of the clonal expansion of virus-specific lymphocytes due to net IL-1-inhibitor activity.