DIFFERENTIAL SENSITIVITY OF MACROPHAGES FROM HERPES-SIMPLEX VIRUS-RESISTANT AND VIRUS-SUSCEPTIBLE MICE TO RESPIRATORY BURST PRIMING BY INTERFERON-ALPHA-BETA
DIFFERENTIAL SENSITIVITY OF MACROPHAGES FROM HERPES-SIMPLEX VIRUS-RESISTANT AND VIRUS-SUSCEPTIBLE MICE TO RESPIRATORY BURST PRIMING BY INTERFERON-ALPHA-BETA
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DOI：
10.1099/0022-1317-70-8-2139
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发表时间：
1989-08-01
影响因子：
3.8
通讯作者：
MOGENSEN, SC
中科院分区：
文献类型：
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作者：
ELLERMANNERIKSEN, S;SOMMERLUND, M;MOGENSEN, SC
单纯疱疹病毒启动小鼠巨噬细胞的基因决定的呼吸爆发，以自分泌方式由干扰素(干扰素)-α/β介导。我们分析了干扰素-α/β的作用。以佛波醇酯为触发剂的鲁米诺依赖化学发光法研究小鼠腹腔巨噬细胞的呼吸爆发能力。巨噬细胞产生的干扰素-α/β。以及纯化的干扰素-α。和-.测试版。有规律地以浓度依赖的方式增强腹膜细胞的呼吸爆发能力。这种增强反应完全是由巨噬细胞介导的，与干扰素α/β孵育4h即可见增强反应，8h达高峰，24 h后逐渐下降至接近本底水平。经干扰素与干扰素-α/β抗血清预先孵育后完全消失。用该抗血清获得的数据表明，内源性干扰素有时是由腹膜细胞自发产生的，而标准的细胞病变抑制试验无法检测到这种内源性干扰素。此外，粗制的巨噬细胞制剂似乎含有一种巨噬细胞失活因子，可以抵消干扰素-α/β的作用。巨噬细胞对α/β干扰素呼吸爆发启动效应敏感性的遗传分析。揭示了该性状是作为共显性常染色体特征遗传的。抗单纯疱疹病毒的C57BL/6小鼠的巨噬细胞比敏感的BALB/c小鼠的巨噬细胞更敏感，而正反交小鼠的巨噬细胞的敏感性介于亲本株之间。不同的干扰素敏感性在抵抗病毒感染方面的生理作用被提出。
Herpes simplex virus primes mouse macrophages for a genetically determined respiratory burst mediated in an autocrine manner by interferon (IFN)-.alpha./.beta.. We have analysed the effect of IFN-.alpha./.beta. on the respiratory burst capacity of mouse peritoneal macrophages by luminol-dependent chemiluminescence using phorbol myristate acetate as trigger. Crude macrophage-produced IFN-.alpha./.beta. as well as purified IFN-.alpha. and -.beta. regularly augmented the respiratory burst capacity of peritoneal cells in a concentration-dependent manner. The augmented response was exclusively mediated by macrophages and was manifest after 4 h incubation with IFN-.alpha./.beta., peaked after 8 h and gradually declined to near background levels after 24 h. The effect of macrophage-produced IFN-.alpha./.beta. was completely abolished by preincubation of IFN with antiserum to IFN-.alpha./.beta.. The data obtained with this antiserum indicated that endogenous IFN, undetectable by a standard cytopathic effect-inhibition assay, was sometimes spontaneously produced by the peritoneal cells. Furthermore, the crude macrophage preparation seemed to contain a macrophage deactivating factor counteracting the effect of IFN-.alpha./.beta.. Genetic analysis of the sensitivity of macrophages for the respiratory burst-priming effect of IFN-.alpha./.beta. revealed that the trait is inherited as a co-dominant autosomal feature. Macrophages from herpes simplex virus-resistant C57BL/6 mice were more sensitive than macrophages from virus-susceptible BALB/c mice and cells from mice of the reciprocal crosses showed an equal sensitivity intermediate between those of the parental strains. A physiological role of differential IFN sensitivity in the context of resistance to virus infections is suggested.