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干扰素-γ与白细胞介素-3和白细胞介素-4在调节小鼠腹腔肥大细胞5-羟色胺和花生四烯酸释放中的相互作用。

Interactions of IFN-gamma with IL-3 and IL-4 in the regulation of serotonin and arachidonate release from mouse peritoneal mast cells.

作者信息

Holliday M R, Banks E M, Dearman R J, Kimber I, Coleman J W

机构信息

Department of Pharmacology and Therapeutics, University of Liverpool, U.K.

出版信息

Immunology. 1994 May;82(1):70-4.

PMID:8045595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1414856/
Abstract

We have examined the interactions between interferon-gamma (IFN-gamma), interleukin-3 (IL-3) and interleukin-4 (IL-4) in the regulation of IgE/antigen-induced secretory responses of mouse peritoneal mast cells. The cytokines were added either alone or in various combinations to cultured mast cells sensitized passively with IgE antibody. In experiments with unfractionated peritoneal cells (containing approx. 1% mast cells), IL-3 and IL-4 enhanced in an additive manner antigen-induced release of serotonin (5-HT), while IFN-gamma inhibited release regardless of whether IL-3 and/or IL-4 were present. In experiments employing mast cells purified to > 90%, IL-3 and IL-4 retained their enhancing activities whereas the inhibitory effect of IFN-gamma was considerably diminished. Nevertheless, IFN-gamma still inhibited significantly IL-4-enhanced secretion. The effects of IL-3 and IL-4 +/- IFN-gamma on arachidonate release were identical to those seen for 5-HT release, indicating that the secretion of both preformed mediators and newly synthesized eicosanoids is regulated in a similar way by these cytokines.

摘要

我们研究了γ干扰素(IFN-γ)、白细胞介素-3(IL-3)和白细胞介素-4(IL-4)在调节IgE/抗原诱导的小鼠腹膜肥大细胞分泌反应中的相互作用。将这些细胞因子单独或以各种组合添加到用IgE抗体被动致敏的培养肥大细胞中。在用未分离的腹膜细胞(约含1%肥大细胞)进行的实验中,IL-3和IL-4以相加的方式增强抗原诱导的5-羟色胺(5-HT)释放,而IFN-γ无论IL-3和/或IL-4是否存在均抑制释放。在使用纯化至>90%的肥大细胞进行的实验中,IL-3和IL-4保留了它们的增强活性,而IFN-γ的抑制作用则大大减弱。然而,IFN-γ仍然显著抑制IL-4增强的分泌。IL-3和IL-4 +/- IFN-γ对花生四烯酸释放的影响与5-HT释放的影响相同,表明这些细胞因子以类似的方式调节预先形成的介质和新合成的类花生酸的分泌。

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本文引用的文献

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Sensitization of mice to chemical allergens modulates the responsiveness of isolated mast cells to IgE-dependent activation.使小鼠对化学变应原致敏可调节分离的肥大细胞对IgE依赖性激活的反应性。
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