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γ干扰素通过影响单核细胞HLA - DR的表达来加速免疫增殖。

Interferon-gamma accelerates immune proliferation via its effect on monocyte HLA-DR expression.

作者信息

Becker S

出版信息

Cell Immunol. 1985 Mar;91(1):301-7. doi: 10.1016/0008-8749(85)90053-x.

DOI:10.1016/0008-8749(85)90053-x
PMID:3918797
Abstract

The effect of interferon-gamma (IFN-gamma) on antigen-induced and autologous proliferative responses has been investigated. The enhanced proliferative response, which resulted in the presence of IFN-gamma, was found to be the consequence of the increased density of HLA-DR induced on the accessory cells. The enhanced proliferation was at least partly due to a shift in the proliferation time course. The response to tetanus toxoid peaked 1-2 days earlier when IFN-gamma-treated monocytes acted as accessory cells than when untreated monocytes presented the antigen. Modulation of the level of DR by preincubation of the monocytes with anti-DR antibody with and without IFN-gamma demonstrated that both autologous and antigen-driven proliferation was influenced in proportion to the level of DR expressed at the time of stimulation. These experiments point to the importance of IFN-gamma in inducing an accelerated immune response via its effect on the density of DR expression on the accessory cell.

摘要

已经研究了γ干扰素(IFN-γ)对抗原诱导的和自身增殖反应的影响。发现IFN-γ存在时增强的增殖反应是辅助细胞上诱导的HLA-DR密度增加的结果。增殖增强至少部分归因于增殖时间进程的改变。当用IFN-γ处理的单核细胞作为辅助细胞时,对破伤风类毒素的反应比未处理的单核细胞呈递抗原时提前1-2天达到峰值。用抗DR抗体在有和没有IFN-γ的情况下对单核细胞进行预孵育来调节DR水平,结果表明自身增殖和抗原驱动的增殖均与刺激时表达的DR水平成比例地受到影响。这些实验表明IFN-γ通过其对辅助细胞上DR表达密度的影响在诱导加速的免疫反应中具有重要作用。

相似文献

1
Interferon-gamma accelerates immune proliferation via its effect on monocyte HLA-DR expression.γ干扰素通过影响单核细胞HLA - DR的表达来加速免疫增殖。
Cell Immunol. 1985 Mar;91(1):301-7. doi: 10.1016/0008-8749(85)90053-x.
2
Antigen presentation by interferon-gamma-treated endothelial cells and fibroblasts: differential ability to function as antigen-presenting cells despite comparable Ia expression.经干扰素-γ处理的内皮细胞和成纤维细胞的抗原呈递:尽管Ia表达相当,但作为抗原呈递细胞发挥功能的能力存在差异。
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Human dermal fibroblasts present tetanus toxoid antigen to antigen-specific T cell clones.人皮肤成纤维细胞将破伤风类毒素抗原呈递给抗原特异性T细胞克隆。
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Regulation of human peripheral blood monocyte DR antigen expression in vitro by lymphokines and recombinant interferons.细胞因子和重组干扰素对人外周血单核细胞DR抗原体外表达的调控
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Pure interferon gamma enhances class II HLA antigens on human monocyte cell lines.纯γ干扰素可增强人单核细胞系上的II类HLA抗原。
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Hydrocortisone-mediated inhibition of monocyte antigen presentation: dissociation of inhibitory effect and expression of DR antigens.氢化可的松介导的单核细胞抗原呈递抑制作用:抑制效应与DR抗原表达的解离
Cell Immunol. 1984 May;85(2):330-9. doi: 10.1016/0008-8749(84)90247-8.

引用本文的文献

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Interferome signature dynamics during the anti-dengue immune response: a systems biology characterization.抗登革免疫反应中干扰组特征的动态变化:系统生物学特征描述。
Front Immunol. 2023 Aug 10;14:1243516. doi: 10.3389/fimmu.2023.1243516. eCollection 2023.
2
Insulin-like growth factor I promotes cord blood T cell maturation through monocytes and inhibits their apoptosis in part through interleukin-6.胰岛素样生长因子I通过单核细胞促进脐血T细胞成熟,并部分通过白细胞介素-6抑制其凋亡。
BMC Immunol. 2008 Dec 17;9:74. doi: 10.1186/1471-2172-9-74.
3
Effect of interferon-gamma on class-II antigen expression and accessory cell function.
γ干扰素对Ⅱ类抗原表达及辅助细胞功能的影响。
Surv Immunol Res. 1985;4(2):135-45. doi: 10.1007/BF02918809.
4
Enhancement of monocyte class I and II histocompatibility antigen expression in man by in vivo beta-interferon.体内β-干扰素增强人体单核细胞I类和II类组织相容性抗原表达
Clin Exp Immunol. 1987 Jul;69(1):107-15.
5
Induction of in vitro autoimmune responses by mononuclear blood cells in Hashimoto's thyroiditis.桥本甲状腺炎中单核血细胞诱导的体外自身免疫反应
Clin Exp Immunol. 1987 Sep;69(3):508-15.
6
Interactions of interferons in the induction of histocompatibility antigens in mouse fibroblasts and glial cells.干扰素在小鼠成纤维细胞和神经胶质细胞中诱导组织相容性抗原的相互作用。
Immunology. 1989 Aug;67(4):537-9.
7
Inducibility of class II major histocompatibility complex antigens by interferon gamma is associated with reduced tumorigenicity in C3H mouse fibroblasts transformed by v-Ki-ras.γ干扰素对II类主要组织相容性复合体抗原的诱导作用与v-Ki-ras转化的C3H小鼠成纤维细胞的致瘤性降低有关。
J Exp Med. 1991 Jan 1;173(1):193-6. doi: 10.1084/jem.173.1.193.