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抑制细胞对单纯疱疹病毒特异性淋巴细胞增殖的调节

Regulation of herpes simplex virus-specific lymphoproliferation by suppressor cells.

作者信息

Horohov D W, Moore R N, Rouse B T

出版信息

J Virol. 1985 Oct;56(1):1-6. doi: 10.1128/JVI.56.1.1-6.1985.

Abstract

We investigated the regulation of the herpes simplex virus (HSV)-specific lymphoproliferative response (LPR) by suppressor cells. The chief cell types in HSV-immune splenocytes proliferating in response to the antigen were Lyt 1+ and Lyt 2+ T cells, which accounted for approximately 60 and 40% of the response, respectively. Because the total responsiveness of splenocytes was enhanced after depletion of Lyt 2+ cells, the LPR was assumed to be subject to regulation by an Lyt 2+ suppressor cell. This was shown to be the case with an experimental design in which suppressor cell activity was induced in one culture, the cells were irradiated, and the effects on LPR were measured in a test antigen-stimulated culture. The cell responsible for suppression was shown to be Lyt 2+ IJ+, and the actual suppressor effect was not antigen specific. Cellular requirements for the generation of suppression were also investigated. The three distinct cell types that appeared to be required were Lyt 2+ and Lyt 1+ T cells and an IJ+ antigen-presenting cell. Of the three cell types, only the Lyt 2+ cell needed to be from HSV-immune animals. The implications of our model system for the better understanding of the role of immunity in herpesvirus pathogenesis are discussed.

摘要

我们研究了抑制细胞对单纯疱疹病毒(HSV)特异性淋巴细胞增殖反应(LPR)的调节作用。对该抗原产生增殖反应的HSV免疫脾细胞中的主要细胞类型是Lyt 1⁺和Lyt 2⁺ T细胞,它们分别约占反应的60%和40%。由于Lyt 2⁺细胞耗竭后脾细胞的总反应性增强,因此推测LPR受Lyt 2⁺抑制细胞的调节。在一种实验设计中证实了这一点,即在一种培养物中诱导抑制细胞活性,对细胞进行照射,然后在经测试抗原刺激的培养物中测量其对LPR的影响。结果表明,负责抑制的细胞是Lyt 2⁺ IJ⁺,实际的抑制作用并非抗原特异性的。我们还研究了产生抑制作用的细胞需求。似乎需要的三种不同细胞类型是Lyt 2⁺和Lyt 1⁺ T细胞以及IJ⁺抗原呈递细胞。在这三种细胞类型中,只有Lyt 2⁺细胞需要来自HSV免疫动物。本文讨论了我们的模型系统对于更好地理解免疫在疱疹病毒发病机制中的作用的意义。

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T-cell growth factor.T细胞生长因子。
Immunol Rev. 1980;51:337-57. doi: 10.1111/j.1600-065x.1980.tb00327.x.
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Suppressor cells and immunoregulation.抑制细胞与免疫调节。
Annu Rev Immunol. 1984;2:127-57. doi: 10.1146/annurev.iy.02.040184.001015.

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