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感染期间集落刺激活性与干扰素产生之间的关系。

Relationship between colony-stimulating activity and interferon production during infection.

作者信息

Egan P, Cheers C

机构信息

Department of Microbiology, University of Melbourne, Parkville, Victoria, Australia.

出版信息

Immunology. 1990 Jun;70(2):191-6.

Abstract

Normal mouse spleen, when cultured in vitro for 3 days in the presence of 10(8) heat-killed Listeria monocytogenes organisms, produced colony-stimulating factors (CSF) that were capable of supporting the production of haemopoietic colonies by bone marrow cells in semi-solid agar, or supporting bone marrow proliferation in liquid medium. In contrast, when the spleen cells were prepared from mice that had been infected with Listeria monocytogenes, colony-stimulating activity (CSA) was no longer detectable over a period from Day 3 to Day 17 post-infection. Suppression of CSA was imposed on normal spleen cells when nylon-wool filtered, T-cell enriched spleen cells from infected mice were co-cultured with normal spleen cells. Suppression largely coincided with the production of interferon by whole spleen from infected mice, and when interferon-gamma (IFN-gamma) was neutralized by antibody CSA was again detected. An early IFN-gamma-independent decrease in CSA production was also detected 2-3 days post-infection. The relevance of this system to the control of CSF production in vivo is discussed.

摘要

正常小鼠脾脏在含有10⁸个热灭活单核细胞增生李斯特菌的条件下体外培养3天,可产生集落刺激因子(CSF),该因子能够在半固体琼脂中支持骨髓细胞产生造血集落,或在液体培养基中支持骨髓增殖。相比之下,当从感染单核细胞增生李斯特菌的小鼠中制备脾细胞时,在感染后第3天至第17天期间不再能检测到集落刺激活性(CSA)。当将感染小鼠经尼龙毛过滤、富含T细胞的脾细胞与正常脾细胞共培养时,正常脾细胞的CSA受到抑制。这种抑制在很大程度上与感染小鼠全脾产生干扰素的情况一致,并且当用抗体中和γ干扰素(IFN-γ)时,再次检测到CSA。在感染后2 - 3天还检测到了CSA产生的早期不依赖IFN-γ的下降。本文讨论了该系统与体内CSF产生控制的相关性。

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