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1
Effect of gamma interferon on cachectin expression by mononuclear phagocytes. Reversal of the lpsd (endotoxin resistance) phenotype.γ干扰素对单核吞噬细胞恶病质素表达的影响。内毒素耐受（Lpsd）表型的逆转。
J Exp Med. 1986 Nov 1;164(5):1791-6. doi: 10.1084/jem.164.5.1791.
2
Interferon-gamma overcomes glucocorticoid suppression of cachectin/tumor necrosis factor biosynthesis by murine macrophages.
J Clin Invest. 1990 Oct;86(4):1234-40. doi: 10.1172/JCI114829.
3
Control of cachectin (tumor necrosis factor) synthesis: mechanisms of endotoxin resistance.恶病质素（肿瘤坏死因子）合成的调控：内毒素耐受机制
Science. 1986 May 23;232(4753):977-80. doi: 10.1126/science.3754653.
4
Endotoxin-induced early gene expression in C3H/HeJ (Lpsd) macrophages.内毒素诱导C3H/HeJ（Lpsd）巨噬细胞中的早期基因表达。
J Immunol. 1994 Sep 15;153(6):2653-63.
5
Effects of different biological response modifiers on interferon expression in bacterial lipopolysaccharide (LPS)-responsive and LPS-hyporesponsive mouse peritoneal macrophages.不同生物反应调节剂对细菌脂多糖（LPS）反应性和LPS低反应性小鼠腹腔巨噬细胞中干扰素表达的影响。
J Gen Virol. 1990 Nov;71 ( Pt 11):2585-91. doi: 10.1099/0022-1317-71-11-2585.
6
Production of tumor necrosis factor by rIFN-gamma-primed C3H/HeJ (Lpsd) macrophages requires the presence of lipid A-associated proteins.经重组干扰素-γ预处理的C3H/HeJ（Lpsd）巨噬细胞产生肿瘤坏死因子需要脂多糖相关蛋白的存在。
J Immunol. 1988 Dec 15;141(12):4196-202.
7
Gamma interferon enhances macrophage transcription of the tumor necrosis factor/cachectin, interleukin 1, and urokinase genes, which are controlled by short-lived repressors.γ干扰素增强巨噬细胞中肿瘤坏死因子/恶病质素、白细胞介素1和尿激酶基因的转录，这些基因受短命阻遏物的调控。
J Exp Med. 1986 Dec 1;164(6):2113-8. doi: 10.1084/jem.164.6.2113.
8
Lipid A-associated proteins provide an alternate "second signal" in the activation of recombinant interferon-gamma-primed, C3H/HeJ macrophages to a fully tumoricidal state.脂多糖A相关蛋白在将重组γ干扰素预处理的C3H/HeJ巨噬细胞激活至完全杀瘤状态的过程中提供了另一种“第二信号”。
J Immunol. 1987 Dec 1;139(11):3697-702.
9
Macrophage/monocyte receptor for nonenzymatically glycosylated protein is upregulated by cachectin/tumor necrosis factor.非酶糖基化蛋白的巨噬细胞/单核细胞受体被恶病质素/肿瘤坏死因子上调。
J Clin Invest. 1989 Dec;84(6):1813-20. doi: 10.1172/JCI114366.
10
Macrophages from endotoxin-hyporesponsive (Lpsd) C3H/HeJ mice are permissive for vesicular stomatitis virus because of reduced levels of endogenous interferon: possible mechanism for natural resistance to virus infection.内毒素低反应性（Lpsd）C3H/HeJ小鼠的巨噬细胞对水疱性口炎病毒具有易感性，原因是内源性干扰素水平降低：这可能是对病毒感染产生天然抵抗力的机制。
J Virol. 1987 Mar;61(3):812-8. doi: 10.1128/JVI.61.3.812-818.1987.

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1
IFN-γ and LPS Induce Synergistic Expression of CCL2 in Monocytic Cells via H3K27 Acetylation.IFN-γ和脂多糖通过H3K27乙酰化诱导单核细胞中CCL2的协同表达。
J Inflamm Res. 2022 Jul 27;15:4291-4302. doi: 10.2147/JIR.S368352. eCollection 2022.
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Science review: key inflammatory and stress pathways in critical illness - the central role of the Toll-like receptors.科学综述：危重症中的关键炎症和应激途径——Toll样受体的核心作用
Crit Care. 2003 Feb;7(1):39-46. doi: 10.1186/cc1828. Epub 2002 Sep 18.
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Enhancement of Mycobacterium tuberculosis-induced tumor necrosis factor alpha production from primary human monocytes by an activated T-cell membrane-mediated mechanism.通过活化T细胞膜介导机制增强结核分枝杆菌诱导的原代人单核细胞肿瘤坏死因子α的产生。
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4
Gamma interferon and lipopolysaccharide interact at the level of transcription to induce tumor necrosis factor alpha expression.γ干扰素和脂多糖在转录水平相互作用，以诱导肿瘤坏死因子α的表达。
Infect Immun. 2001 May;69(5):2847-52. doi: 10.1128/IAI.69.5.2847-2852.2001.
5
Toll-like receptors: molecular mechanisms of the mammalian immune response.Toll样受体：哺乳动物免疫反应的分子机制
Immunology. 2000 Sep;101(1):1-10. doi: 10.1046/j.1365-2567.2000.00093.x.
6
Regulation of matrix metalloproteinases and their inhibitor genes in lipopolysaccharide-induced endotoxemia in mice.小鼠脂多糖诱导的内毒素血症中基质金属蛋白酶及其抑制基因的调控
Am J Pathol. 2000 Jul;157(1):197-210. doi: 10.1016/S0002-9440(10)64531-2.
7
Interferon-gamma and tumor necrosis factor-alpha determine resistance to Paracoccidioides brasiliensis infection in mice.干扰素-γ和肿瘤坏死因子-α决定小鼠对巴西副球孢子菌感染的抵抗力。
Am J Pathol. 2000 May;156(5):1811-20. doi: 10.1016/s0002-9440(10)65053-5.
8
Differential expression of inducible nitric oxide synthase gene by alveolar and peritoneal macrophages in lipopolysaccharide-hyporesponsive C3H/HeJ mice.脂多糖低反应性C3H/HeJ小鼠肺泡巨噬细胞和腹腔巨噬细胞中诱导型一氧化氮合酶基因的差异表达
Immunology. 1999 Dec;98(4):497-503. doi: 10.1046/j.1365-2567.1999.00908.x.
9
Interferon-gamma (IFN-gamma) and prostaglandin E2 (PGE2) regulate differently IL-12 production in human intestinal lamina propria mononuclear cells (LPMC).干扰素-γ（IFN-γ）和前列腺素E2（PGE2）对人肠道固有层单核细胞（LPMC）中白细胞介素-12（IL-12）的产生有不同的调节作用。
Clin Exp Immunol. 1999 Sep;117(3):469-75. doi: 10.1046/j.1365-2249.1999.00991.x.
10
Lipopolysaccharides (LPS) of oral black-pigmented bacteria induce tumor necrosis factor production by LPS-refractory C3H/HeJ macrophages in a way different from that of Salmonella LPS.口腔产黑色素菌的脂多糖以不同于沙门氏菌脂多糖的方式，诱导LPS耐受的C3H/HeJ巨噬细胞产生肿瘤坏死因子。
Infect Immun. 1999 Apr;67(4):1736-42. doi: 10.1128/IAI.67.4.1736-1742.1999.

本文引用的文献

1
Recombinant interferons increase macrophage Fc receptor capacity.重组干扰素可提高巨噬细胞Fc受体的能力。
J Immunol. 1984 May;132(5):2436-9.
2
Identification of interferon-gamma as the lymphokine that activates human macrophage oxidative metabolism and antimicrobial activity.鉴定γ干扰素为激活人类巨噬细胞氧化代谢和抗菌活性的淋巴因子。
J Exp Med. 1983 Sep 1;158(3):670-89. doi: 10.1084/jem.158.3.670.
3
Macrophage activation: priming activity from a T-cell hybridoma is attributable to interferon-gamma.巨噬细胞激活：来自T细胞杂交瘤的启动活性归因于γ干扰素。
Proc Natl Acad Sci U S A. 1983 Jun;80(12):3782-6. doi: 10.1073/pnas.80.12.3782.
4
Recombinant mouse gamma interferon induces the priming step in macrophage activation for tumor cell killing.重组小鼠γ干扰素在巨噬细胞激活以杀伤肿瘤细胞的过程中诱导启动步骤。
J Immunol. 1983 May;130(5):2011-3.
5
Endogenous interferon production by endotoxin-responsive macrophages provides an autostimulatory differentiation signal.内毒素反应性巨噬细胞产生的内源性干扰素提供了一种自身刺激分化信号。
Infect Immun. 1984 Aug;45(2):417-23. doi: 10.1128/iai.45.2.417-423.1984.
6
Activation of human macrophages. Comparison of other cytokines with interferon-gamma.人巨噬细胞的激活。其他细胞因子与γ干扰素的比较。
J Exp Med. 1984 Aug 1;160(2):600-5. doi: 10.1084/jem.160.2.600.
7
A method for isolation of intact, translationally active ribonucleic acid.一种分离完整的、具有翻译活性的核糖核酸的方法。
DNA. 1983;2(4):329-35. doi: 10.1089/dna.1983.2.329.
8
Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule.一种干扰素样分子对C3H/HeJ小鼠巨噬细胞分化缺陷的纠正作用。
J Immunol. 1982 Jan;128(1):380-7.
9
The primary role of lymphoreticular cells in the mediation of host responses to bacterial endotoxim.淋巴网状细胞在介导宿主对细菌内毒素反应中的主要作用。
J Infect Dis. 1980 Jan;141(1):55-63. doi: 10.1093/infdis/141.1.55.
10
Efficient in vitro synthesis of biologically active RNA and RNA hybridization probes from plasmids containing a bacteriophage SP6 promoter.从含有噬菌体SP6启动子的质粒中高效体外合成生物活性RNA和RNA杂交探针。
Nucleic Acids Res. 1984 Sep 25;12(18):7035-56. doi: 10.1093/nar/12.18.7035.

γ干扰素对单核吞噬细胞恶病质素表达的影响。内毒素耐受（Lpsd）表型的逆转。

Effect of gamma interferon on cachectin expression by mononuclear phagocytes. Reversal of the lpsd (endotoxin resistance) phenotype.

作者信息

Beutler B, Tkacenko V, Milsark I, Krochin N, Cerami A

出版信息

J Exp Med. 1986 Nov 1;164(5):1791-6. doi: 10.1084/jem.164.5.1791.

DOI:10.1084/jem.164.5.1791
PMID:3095481
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2188450/
Abstract

IFN-gamma permits the endotoxin-induced production of cachectin by C3H/HeJ (endotoxin resistant) macrophages, apparently by facilitating endotoxin-induced cachectin biosynthesis at both transcriptional and posttranscriptional levels. IFN-gamma cannot induce cachectin biosynthesis by itself, nor does it markedly enhance cachectin production by endotoxin-induced peritoneal macrophages obtained from endotoxin-responsive mice. Elucidation of the precise mechanism through which IFN-gamma influences cachectin biosynthesis may permit a better understanding of the molecular events that follow endotoxin-induced activation of macrophages. Moreover, the permissive effect of IFN-gamma on cachectin biosynthesis might elicit enhanced endotoxin sensitivity in vivo.

摘要

γ干扰素可使C3H/HeJ（对内毒素耐受）巨噬细胞产生内毒素诱导的恶病质素，这显然是通过在转录和转录后水平促进内毒素诱导的恶病质素生物合成来实现的。γ干扰素本身不能诱导恶病质素的生物合成，对于从对内毒素敏感的小鼠获得的内毒素诱导的腹腔巨噬细胞，它也不会显著增强恶病质素的产生。阐明γ干扰素影响恶病质素生物合成的确切机制，可能有助于更好地理解内毒素诱导巨噬细胞活化后发生的分子事件。此外，γ干扰素对恶病质素生物合成的允许作用可能会引起体内对内毒素敏感性的增强。