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具有抗病毒活性的T淋巴细胞进入病毒感染小鼠的胸腺。

Entry of antivirally active T lymphocytes into the thymus of virus-infected mice.

作者信息

Gossmann J, Löhler J, Lehmann-Grube F

机构信息

Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Universität Hamburg, Federal Republic of Germany.

出版信息

J Immunol. 1991 Jan 1;146(1):293-7.

PMID:1898603
Abstract

The thymus has long been regarded as an immunologically "privileged site" by being shielded against the entry of exogenous Ag as well as protective elements of the immune system. After i.p. infection of mice, the lymphocytic choriomeningitis virus multiplied in this organ. Viral Ag was found predominantly in the epithelial-reticular cells of the medulla and to a lesser extent in such cells of the cortex. Beginning on day 7 after infection, the virus disappeared, a process that could be blocked by depleting the mice of peripheral T lymphocytes or of CD8+ cytotoxic T lymphocytes. Viral clearance was accelerated by i.v. injection of splenocytes from mice, which themselves were just eliminating the virus. CD8+ cells from CD8-congenic donor mice, most with blast morphology, were detected immunocytochemically in the thymus, predominantly in the medulla. A few CD8+ T lymphocytes from donors not previously infected were also demonstrated in the thymic tissue of infected mice. Our findings indicate that the lymphocytic choriomeningitis virus has access to the thymus and suggest that it is cleared by the antiviral activity of circulating cytotoxic T lymphocytes. Thus, just as other organs, the thymus appears to be subject to immune surveillance by mature T lymphocytes that have their origin in secondary lymphoid tissues.

摘要

长期以来,胸腺一直被视为免疫“特权部位”,因为它对外源抗原以及免疫系统的保护成分的进入具有屏蔽作用。经腹腔感染小鼠后,淋巴细胞性脉络丛脑膜炎病毒在该器官中增殖。病毒抗原主要在髓质的上皮网状细胞中发现,在皮质的此类细胞中发现的较少。感染后第7天开始,病毒消失,这个过程可通过耗尽小鼠外周T淋巴细胞或CD8 + 细胞毒性T淋巴细胞来阻断。静脉注射自身刚清除病毒的小鼠脾细胞可加速病毒清除。在胸腺中通过免疫细胞化学检测到来自CD8同基因供体小鼠的CD8 + 细胞,大多数具有母细胞形态,主要在髓质中。在感染小鼠的胸腺组织中也证实了一些来自未预先感染的供体的CD8 + T淋巴细胞。我们的研究结果表明,淋巴细胞性脉络丛脑膜炎病毒可进入胸腺,并表明它是通过循环细胞毒性T淋巴细胞的抗病毒活性清除的。因此,正如其他器官一样,胸腺似乎受到起源于二级淋巴组织的成熟T淋巴细胞的免疫监视。

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