MIF-like activity of natural and recombinant human interferon-gamma and their neutralization by monoclonal antibody.

MIF-like activity of natural and recombinant human interferon-gamma and their neutralization by monoclonal antibody.
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天然和重组人干扰素-γ 的 MIF 样活性及其单克隆抗体的中和作用。

DOI:
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发表时间:
1985
影响因子:
4.4
通讯作者:
H. Stevenson
H. Stevenson
中科院分区:
医学2区
文献类型:
--
作者:
G. Thurman;I. Braude;P. Gray;R. Oldham;H. Stevenson

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被引文献

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通过利用淘洗纯化的人单核细胞,我们发现,人干扰素(IFN)抑制单核细胞迁移的方式类似于迁移抑制因子(MIF),它没有明显的细胞毒性。我们观察到,人IFN-γ的MIF活性比IFN-α强10至300倍,单克隆抗体(MoAb)可用于区分它们。用重组IFN-γ进行的研究表明,用天然IFN-γ观察到的迁移抑制是由于IFN-γ本身,而不是由于另一种淋巴因子与天然IFN-γ的共纯化。虽然干扰素具有MIF活性,但显然还有其他没有抗病毒活性的细胞因子也具有MIF活性。来自淋巴母细胞样细胞系RPMI 1788的MIF不被IFN的MoAb中和。然而,从人外周血淋巴细胞培养物的上清液中的MIF活性与Con A-Sepharose刺激完全中和单克隆抗体抗IFN-γ。这些数据表明,MIF确实是一个家族的细胞因子,抑制巨噬细胞/单核细胞迁移和有丝分裂原刺激的淋巴细胞的粗上清液相关的MIF活性的主要部分是由于IFN-γ。
By utilizing elutriation-purified human monocytes, we found that human interferon (IFN) inhibits monocyte migration in a manner similar to migration inhibitory factor (MIF) and does it without demonstrable cytotoxicity. We observed that human IFN-gamma is 10 to 300 times more potent in its MIF activity than is IFN-alpha and that monoclonal antibodies (MoAb) can be used to distinguish between them. Studies with recombinant IFN-gamma indicate that the migration inhibition seen with natural IFN-gamma is due to IFN-gamma itself and is not due to co-purification of another lymphokine with the natural IFN-gamma. Although interferons exhibit MIF activities, there are apparently other cytokines, without antiviral activity, that also have MIF activities. MIF from the lymphoblastoid cell line RPMI 1788 was not neutralized by MoAb to IFN. However, MIF activity in supernatant fluid from human peripheral blood lymphocyte cultures stimulated with Con A-Sepharose was completely neutralized with MoAb anti-IFN-gamma. These data indicate that MIF is really a family of cytokines that inhibit macrophage/monocyte migration and that the major portion of MIF activity associated with crude supernatant of mitogen-stimulated lymphocytes is due to IFN-gamma.