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Infect Immun. 1985 Dec;50(3):765-70. doi: 10.1128/iai.50.3.765-770.1985.
2
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本文引用的文献

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A THREE-CELL INTERACTION REQUIRED FOR THE INDUCTION OF THE PRIMARY IMMUNE RESPONSE in vitro.体外诱导初次免疫反应所需的三细胞相互作用。
Proc Natl Acad Sci U S A. 1968 Oct;61(2):542-7. doi: 10.1073/pnas.61.2.542.
2
Identification and characterization of an exotoxin from Staphylococcus aureus associated with toxic-shock syndrome.与中毒性休克综合征相关的金黄色葡萄球菌外毒素的鉴定与特性分析
J Infect Dis. 1981 Apr;143(4):509-16. doi: 10.1093/infdis/143.4.509.
3
Cell-cell interactions in the T cell proliferative response. I. Analysis of the cell types involved and evidence for nonspecific T cell recruitment.T细胞增殖反应中的细胞间相互作用。I. 所涉及细胞类型的分析及非特异性T细胞募集的证据。
J Immunol. 1980 Aug;125(2):491-500.
4
Accessory function of human tumor cell lines. I. Production of interleukin 1 by the human histiocytic lymphoma cell line U-937.人类肿瘤细胞系的辅助功能。I. 人组织细胞淋巴瘤细胞系U-937产生白细胞介素1
Eur J Immunol. 1982 Oct;12(10):895-9. doi: 10.1002/eji.1830121018.
5
Purification and some physicochemical properties of toxic-shock toxin.中毒性休克毒素的纯化及某些物理化学性质
Biochemistry. 1983 Aug 2;22(16):3907-12. doi: 10.1021/bi00285a028.
6
Induction of human interleukin-1 by a product of Staphylococcus aureus associated with toxic shock syndrome.金黄色葡萄球菌一种与中毒性休克综合征相关的产物诱导人白细胞介素-1的产生。
J Clin Invest. 1984 May;73(5):1312-20. doi: 10.1172/JCI111334.
7
1 alpha,25-dihydroxyvitamin D3 induces maturation of the human monocyte cell line U937, and, in association with a factor from human T lymphocytes, augments production of the monokine, mononuclear cell factor.1α,25-二羟维生素D3诱导人单核细胞系U937成熟,并与人T淋巴细胞来源的一种因子协同作用,增强单核因子即单核细胞因子的产生。
J Clin Invest. 1984 Mar;73(3):731-9. doi: 10.1172/JCI111266.
8
A transplantable myelomonocytic leukemia in BALB-c mice: cytology, karyotype, and muramidase content.BALB-c小鼠中的一种可移植性骨髓单核细胞白血病:细胞学、核型及溶菌酶含量
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9
Promotion of replication in lymphoid cells by specific thiols and disulfides in vitro. Effects on mouse lymphoma cells in comparison with splenic lymphocytes.体外特定硫醇和二硫化物对淋巴样细胞复制的促进作用。与脾淋巴细胞相比,对小鼠淋巴瘤细胞的影响。
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10
Isolation of mononuclear cells and granulocytes from human blood. Isolation of monuclear cells by one centrifugation, and of granulocytes by combining centrifugation and sedimentation at 1 g.从人血中分离单核细胞和粒细胞。通过一次离心分离单核细胞,通过离心和1g沉降相结合的方法分离粒细胞。
Scand J Clin Lab Invest Suppl. 1968;97:77-89.

已建立的巨噬细胞样细胞系在响应中毒性休克综合征毒素时会合成白细胞介素-1。

Established macrophagelike cell lines synthesize interleukin-1 in response to toxic shock syndrome toxin.

作者信息

Hirose A, Ikejima T, Gill D M

出版信息

Infect Immun. 1985 Dec;50(3):765-70. doi: 10.1128/iai.50.3.765-770.1985.

DOI:10.1128/iai.50.3.765-770.1985
PMID:3877692
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC261146/
Abstract

Toxic shock syndrome toxin is already known to induce the production of interleukin-1 (IL-1) by preparations of monocytes and macrophages that are presumably contaminated with other types of cells. The response is enhanced by increasing the density of such monocytes, suggesting that the monocyte's response to toxic shock syndrome toxin may be augmented by its interaction with some other cell. Nevertheless, we now show that several human and murine macrophagelike cell lines (U937, J774, P388D1, and WEHI 3) produce IL-1 when exposed to toxic shock syndrome toxin, and therefore the basic response does not require the presence of cells of other lineages. The cultured cells generally produce less IL-1 than do monocytes, but considerably more IL-1 is induced from cells that have undergone a terminal differentiation as a result of exposure to 1 alpha,25-dihydroxyvitamin D3. High concentrations of cultured cels suppress the production of IL-1; this effect is apparently not due to long-lived inhibitors of IL-1 production or of IL-1 activity, but may be due to a short-lived inhibitor of production.

摘要

毒性休克综合征毒素已知可诱导单核细胞和巨噬细胞制剂产生白细胞介素-1(IL-1),这些制剂可能被其他类型的细胞污染。通过增加此类单核细胞的密度可增强这种反应,这表明单核细胞对毒性休克综合征毒素的反应可能会因其与其他某种细胞的相互作用而增强。然而,我们现在表明,几种人和小鼠的巨噬细胞样细胞系(U937、J774、P388D1和WEHI 3)在暴露于毒性休克综合征毒素时会产生IL-1,因此基本反应并不需要其他谱系的细胞存在。培养的细胞通常比单核细胞产生的IL-1少,但由于暴露于1α,25-二羟基维生素D3而经历终末分化的细胞可诱导产生更多的IL-1。高浓度的培养细胞会抑制IL-1的产生;这种效应显然不是由于IL-1产生或IL-1活性的长效抑制剂,而是可能由于一种产生的短效抑制剂。