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重组干扰素-γ可增加HLA-DR的合成与表达。

Recombinant interferon-gamma increases HLA-DR synthesis and expression.

作者信息

Basham T Y, Merigan T C

出版信息

J Immunol. 1983 Apr;130(4):1492-4.

PMID:6403609
Abstract

It has been shown that all three classes of interferons enhance the expression of the major histocompatibility class I antigens (HLA-A,B,C;H-2) on a wide variety of cell types (1-10). However, their effect on the expression of the class II antigens (HLA-DR, Ia), which play a major part in cellular interactions that initiate an immune response, is more controversial. The predominate findings have been that the interferons specifically increase the synthesis and expression of only the class I antigens (3, 4, 6, 8, 10, 11). We report here that recombinant interferon-gamma (IFN-gamma) increases the synthesis and expression of the HLA-DR (la-like) antigens as well as beta 2-microglobulin (beta 2-m), a low m.w. subunit of HLA, on human melanoma cells. No increase in HLA-DR was detected on these melanoma cells with leukocyte interferon (IFN-alpha) at doses 400 times higher than the maximum dose of IFN-gamma. These findings were extended to show that pure IFN-gamma also increases the expression of the HLA-DR antigens on normal peripheral blood monocytes, whereas recombinant IFN-alpha at a similar dose had little effect on the expression of this surface antigen. These findings suggest a specialized role for IFN-gamma in immune regulation in comparison with IFN-alpha.

摘要

已表明,所有三类干扰素均可增强多种细胞类型上主要组织相容性复合体I类抗原(HLA - A、B、C;H - 2)的表达(1 - 10)。然而,它们对II类抗原(HLA - DR、Ia)表达的影响更具争议性,II类抗原在引发免疫反应的细胞相互作用中起主要作用。主要研究结果表明,干扰素仅特异性增加I类抗原的合成和表达(3、4、6、8、10、11)。我们在此报告,重组干扰素 - γ(IFN - γ)可增加人黑色素瘤细胞上HLA - DR(类Ia)抗原以及β2 - 微球蛋白(β2 - m,HLA的低分子量亚基)的合成和表达。在这些黑色素瘤细胞上,使用比IFN - γ最大剂量高400倍的白细胞干扰素(IFN - α)未检测到HLA - DR增加。这些发现进一步表明,纯IFN - γ也可增加正常外周血单核细胞上HLA - DR抗原的表达,而相似剂量的重组IFN - α对该表面抗原的表达几乎没有影响。与IFN - α相比,这些发现提示IFN - γ在免疫调节中具有特殊作用。

相似文献

1
Recombinant interferon-gamma increases HLA-DR synthesis and expression.重组干扰素-γ可增加HLA-DR的合成与表达。
J Immunol. 1983 Apr;130(4):1492-4.
2
Recombinant interferon-gamma can induce the expression of HLA-DR and -DC on DR-negative melanoma cells and enhance the expression of HLA-ABC and tumor-associated antigens.重组干扰素-γ可诱导DR阴性黑色素瘤细胞上HLA-DR和-DC的表达,并增强HLA-ABC和肿瘤相关抗原的表达。
Eur J Immunol. 1985 Feb;15(2):118-23. doi: 10.1002/eji.1830150204.
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Cloned human interferon-gamma, but not interferon-beta or -alpha, induces expression of HLA-DR determinants by fetal monocytes and myeloid leukemic cell lines.克隆的人γ干扰素可诱导胎儿单核细胞和髓系白血病细胞系表达HLA - DR决定簇,而β干扰素或α干扰素则无此作用。
J Immunol. 1984 Jan;132(1):240-5.
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HLA-DR synthesis induction and expression in HLA-DR-negative carcinoma cell lines of diverse origins by interferon-gamma but not by interferon-beta.γ干扰素而非β干扰素可诱导不同来源的HLA - DR阴性癌细胞系合成并表达HLA - DR。
J Natl Cancer Inst. 1985 Jun;74(6):1261-8.
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Effect of recombinant human leukocyte, fibroblast, and immune interferons on expression of class I and II major histocompatibility complex and invariant chain in early passage human melanoma cells.重组人白细胞、成纤维细胞和免疫干扰素对早期传代人黑素瘤细胞中I类和II类主要组织相容性复合体及恒定链表达的影响。
Cancer Res. 1990 Dec 1;50(23):7422-9.
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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。
Eur J Immunol. 1984 Jan;14(1):106-8. doi: 10.1002/eji.1830140120.
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Interferons as modulators of human monocyte-macrophage differentiation. I. Interferon-gamma increases HLA-DR expression and inhibits phagocytosis of zymosan.干扰素作为人类单核细胞-巨噬细胞分化的调节剂。I. 干扰素-γ增加HLA-DR表达并抑制酵母聚糖的吞噬作用。
J Immunol. 1984 Mar;132(3):1249-54.
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All human monocytes have the capability of expressing HLA-DQ and HLA-DP molecules upon stimulation with interferon-gamma.所有人类单核细胞在受到γ干扰素刺激后都有表达HLA-DQ和HLA-DP分子的能力。
J Immunol. 1986 Jul 15;137(2):519-24.
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Immunochemical and functional analysis of HLA class II antigens induced by recombinant immune interferon on normal epidermal melanocytes.重组免疫干扰素诱导正常表皮黑素细胞产生的HLA-II类抗原的免疫化学及功能分析
J Immunol. 1987 Feb 15;138(4):1310-6.
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Regulation of the antigenic phenotype of human melanoma cells by recombinant interferons.重组干扰素对人黑色素瘤细胞抗原表型的调节
Anticancer Res. 1986 Sep-Oct;6(5):877-84.

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