Nebulized IFN-gamma inhibits the development of secondary allergic responses in mice.
Nebulized IFN-gamma inhibits the development of secondary allergic responses in mice.
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DOI：
10.4049/jimmunol.157.4.1432
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发表时间：
1996-08
影响因子：
4.4
通讯作者：
G. Lack;K. Bradley;Eckard Hamelmann;H. Renz;J. Loader;D. Leung;G. Larsen;E. Gelfand
中科院分区：
文献类型：
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作者：
G. Lack;K. Bradley;Eckard Hamelmann;H. Renz;J. Loader;D. Leung;G. Larsen;E. Gelfand
研究了雾化IFN-γ对原发性和继发性IgE产生以及气道高反应性（AHR）发展的影响。BALB/c小鼠每天接受初次暴露于雾化的OVA，持续10天，并在第12天测定时产生抗OVA IgE应答、对OVA的立即皮肤反应性和气道功能改变。在第30天和第31天二次暴露于OVA激发后，这些小鼠在第37天测量时产生了放大的IgE应答，对OVA和AHR的皮肤反应性升高。在初次OVA致敏前3天和期间开始给予IFN-γ 13天，导致抗OVA IgE降低，血清抗OVA IgG 2a水平升高，皮肤对OVA的反应性降低，初次致敏后第12天评估时气道功能正常。该处理还防止了继发性抗OVA IgE应答的发展和气道反应性的改变，但在第37天测量的血清中未诱导抗OVA IgG 2a的继发性升高。在第26至30天，在初步应答建立后很久，但就在二次OVA攻击之前，用IFN-γ治疗，消除了二次抗OVA IgE应答的发展，导致血清中抗OVA IgG 2a的增加，并防止了AHR的发展。在体外，从用“早期”或“晚期”IFN-γ处理的OVA致敏小鼠中获得的CD 4 + T细胞抑制IgE的产生。IFN-γ向气道的递送可以防止继发性过敏原致敏，即使在已经实现原发性致敏之后，并且这种作用由CD 4 + T细胞介导。
The effects of nebulized IFN-gamma on primary and secondary IgE production and development of airway hyper-responsiveness (AHR) were investigated. BALB/c mice received primary exposure to aerosolized OVA daily for 10 days and developed anti-OVA IgE responses, immediate cutaneous reactivity to OVA, and altered airway function when assayed on day 12. After secondary exposure to OVA challenges on days 30 and 31, these mice developed an amplified IgE response, heightened cutaneous reactivity to OVA and AHR when measured on day 37. Administration of IFN-gamma for 13 days, beginning 3 days prior to and during primary OVA sensitization, resulted in a decrease in anti-OVA IgE, increases in serum anti-OVA IgG2a levels, a decrease in cutaneous reactivity to OVA, and normal airway function when assessed on day 12 after primary sensitization. This treatment also prevented the development of secondary anti-OVA IgE responses and altered airway responsiveness but did not induce a secondary rise in anti-OVA IgG2a in the serum measured on day 37. Treatment with IFN-gamma on days 26 to 30, well after primary responses were established but just prior to secondary OVA challenge, abolished the development of secondary anti-OVA IgE responses, resulted in an increase in anti-OVA IgG2a in the serum, and prevented the development of AHR. In vitro, CD4+ T cells obtained from OVA-sensitized mice treated with either "early" or "late" IFN-gamma inhibited IgE production. Delivery of IFN-gamma to the airways can prevent secondary allergen sensitization even after primary sensitization has been achieved and this effect is mediated by CD4+ T cells.