Transfer of the enhancing effect of respiratory syncytial virus infection on subsequent allergic airway sensitization by T lymphocytes.
Transfer of the enhancing effect of respiratory syncytial virus infection on subsequent allergic airway sensitization by T lymphocytes.
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DOI：
10.4049/jimmunol.163.10.5729
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发表时间：
1999-11
影响因子：
4.4
通讯作者：
J. Schwarze;M. Mäkelä;G. Cieslewicz;A. Dakhama;M. Lahn;T. Ikemura;A. Joetham;E. Gelfand
中科院分区：
文献类型：
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作者：
J. Schwarze;M. Mäkelä;G. Cieslewicz;A. Dakhama;M. Lahn;T. Ikemura;A. Joetham;E. Gelfand
在小鼠中，呼吸道合胞病毒（RSV）感染增强了过敏性气道致敏，导致肺嗜酸性粒细胞增多和气道高反应性（AHR）。RSV促进哮喘发展的机制及其对小鼠过敏性气道致敏的影响尚不清楚。我们测试了RSV感染的这些后果是否可以通过T细胞过继转移，以及T细胞亚群的消耗是否可以阻止RSV感染对随后气道致敏的影响。将rsv感染小鼠的支气管周围淋巴结（PBLN）的单核细胞、T淋巴细胞或CD4或CD8 T细胞转移到幼稚的BALB/c小鼠中，然后通过气道暴露于OVA。此外，RSV感染小鼠在急性RSV感染后，但在气道致敏之前，CD4或CD8 T细胞被耗尽。致敏后，监测气道对吸入甲胆碱的反应性、肺嗜酸性粒细胞的数量以及PBLN细胞培养中ifn - γ、IL-4和IL-5的水平。来自rsv感染小鼠的T细胞转移导致嗜酸性粒细胞流入肺部增加，IL-5产生增加，气道致敏后发生AHR。暴露于卵细胞10天后，从rsv感染小鼠的PBLN转移CD8而不是CD4 T细胞也会导致AHR。此外，CD8 T细胞的耗竭阻止了RSV感染的这些后果，而CD4 T细胞的耗竭则减少了这些后果。我们的结论是，T细胞，特别是CD8 T细胞，在rsv诱导的过敏性气道致敏后肺嗜酸性粒细胞增多和AHR的发展中起关键作用。
In mice, respiratory syncytial virus (RSV) infection enhances allergic airway sensitization, resulting in lung eosinophilia and in airway hyperresponsiveness (AHR). The mechanisms by which RSV contributes to development of asthma and its effects on allergic airway sensitization in mice are not known. We tested whether these consequences of RSV infection can be adoptively transferred by T cells and whether depletion of T cell subsets prevents the effects of RSV infection on subsequent airway sensitization. Mononuclear cells, T lymphocytes, or CD4 or CD8 T cells from peribronchial lymph nodes (PBLN) of RSV-infected mice were transferred into naive BALB/c mice which were then exposed to OVA via the airways. Additionally, RSV-infected mice were depleted of CD4 or CD8 T cells following acute RSV infection but prior to airway sensitization. Following sensitization, airway responsiveness to inhaled methacholine, numbers of lung eosinophils, and levels of IFN-gamma, IL-4, and IL-5 in PBLN cell cultures were monitored. Transfer of T cells from RSV-infected mice resulted in increased eosinophil influx into the lungs, increased IL-5 production, and development of AHR following airway sensitization to allergen. Transfer of CD8 but not CD4 T cells from the PBLN of RSV-infected mice also resulted in AHR following 10 days of OVA exposure. Further, depletion of CD8 T cells prevented these consequences of RSV infection while CD4 T cell depletion reduced them. We conclude that T cells, in particular CD8 T cells, are critical in mediating RSV-induced development of lung eosinophilia and AHR following allergic airway sensitization.