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白细胞介素-4抑制刺激后的人单核细胞中粒细胞集落刺激因子和粒细胞-巨噬细胞集落刺激因子的水平。

Interleukin-4 suppresses granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor levels in stimulated human monocytes.

作者信息

Hamilton J A, Whitty G A, Royston A K, Cebon J, Layton J E

机构信息

University of Melbourne, Department of Medicine, Parkville, Australia.

出版信息

Immunology. 1992 Aug;76(4):566-71.

PMID:1383133
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1421558/
Abstract

Granulocyte colony-stimulating factor (G-CSF) was quantitated in the supernatants of lipopolysaccharide (LPS)-treated human monocytes by ELISA. Unlike previous reports, the lymphokines, interleukin-4 (IL-4) and interferon-gamma (IFN-gamma), were unable to induce the synthesis of G-CSF. Both IL-4 (> or = 10 pM) and the glucocorticoid, dexamethasone (10(-7) M), inhibited G-CSF production in the LPS-treated monocytes; in contrast, IFN-gamma had a weak potentiating effect on the LPS action. Changes in antigen expression were manifested at the level of messenger RNA (mRNA). Granulocyte-macrophage (GM)-CSF in the LPS-treated monocyte supernatants was also quantitated by ELISA but its levels were somewhat lower than for G-CSF; IL-4, dexamethasone and IFN-gamma had similar effects on GM-CSF levels as on G-CSF levels. The suppression of CSF production in the stimulated monocytes by IL-4 and glucocorticoid extends the list of monocyte cytokines whose levels can be down-regulated by these agents and suggests another potential anti-inflammatory and immunosuppressive function for IL-4.

摘要

采用酶联免疫吸附测定法(ELISA)对脂多糖(LPS)处理的人单核细胞培养上清液中的粒细胞集落刺激因子(G-CSF)进行定量分析。与先前的报道不同,淋巴因子白细胞介素-4(IL-4)和干扰素-γ(IFN-γ)无法诱导G-CSF的合成。IL-4(≥10 pM)和糖皮质激素地塞米松(10⁻⁷ M)均抑制LPS处理的单核细胞中G-CSF的产生;相反,IFN-γ对LPS的作用有微弱的增强作用。抗原表达的变化在信使核糖核酸(mRNA)水平上得以体现。同样采用ELISA对LPS处理的单核细胞培养上清液中的粒细胞-巨噬细胞(GM)-CSF进行定量分析,但其水平略低于G-CSF;IL-4、地塞米松和IFN-γ对GM-CSF水平的影响与对G-CSF水平的影响相似。IL-4和糖皮质激素对受刺激单核细胞中CSF产生的抑制作用,扩展了可被这些因子下调水平的单核细胞细胞因子的种类,并提示IL-4具有另一种潜在的抗炎和免疫抑制功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4b/1421558/38a8a6f7e3a0/immunology00107-0057-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4b/1421558/255c4a31c715/immunology00107-0056-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4b/1421558/38a8a6f7e3a0/immunology00107-0057-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4b/1421558/255c4a31c715/immunology00107-0056-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4b/1421558/38a8a6f7e3a0/immunology00107-0057-a.jpg

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