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干扰素临床应用的生物学基础。

The biological basis for clinical use of interferon.

作者信息

Dianzani F, Antonelli G, Capobianchi M R

机构信息

Institute of Virology, University La Sapienza, Rome, Italy.

出版信息

J Hepatol. 1990;11 Suppl 1:S5-10. doi: 10.1016/0168-8278(90)90156-l.

Abstract

Interferons represent the body's most rapid defence against virus infection. Natural recovery from viral infections is correlated with interferon production; the inhibition of interferon enhances the severity of infection and interferon has been shown to protect animals from some viral infections. beta-Interferon is produced by fibroblasts in response to viral infection. Leucocyte (a) interferon may be induced by foreign or infected cells or by viruses, and it is continuously released into the bloodstream during infection, declining with time. gamma-Interferon are produced later in viral infection by virus-sensitized T lymphocytes. The antiviral action of interferon is induced by interaction with specific receptors on cell surfaces leading to translation of antiviral proteins. Interferons may also enhance immune responses by increasing expression of lymphocyte surface antigens and by increasing the cytotoxic activity of natural killer cells. In chronic hepatitis B and C, it seems likely that interferon's antiviral activity is responsible for the early fall of viral products, while its immunomodulatory activity is responsible for long-term effects, including the destruction of infected hepatocytes, with persistent loss of viral antigens and seroconversion.

摘要

干扰素是人体对病毒感染最迅速的防御机制。从病毒感染中自然恢复与干扰素的产生相关;对干扰素的抑制会加重感染的严重程度,并且已证明干扰素能保护动物免受某些病毒感染。β干扰素由成纤维细胞在病毒感染时产生。白细胞(α)干扰素可由外来或受感染的细胞或病毒诱导产生,在感染期间它会持续释放到血液中,并随时间下降。γ干扰素在病毒感染后期由对病毒敏感的T淋巴细胞产生。干扰素的抗病毒作用是通过与细胞表面的特定受体相互作用诱导产生的,从而导致抗病毒蛋白的翻译。干扰素还可通过增加淋巴细胞表面抗原的表达以及增强自然杀伤细胞的细胞毒性活性来增强免疫反应。在慢性乙型和丙型肝炎中,干扰素的抗病毒活性似乎导致病毒产物的早期下降,而其免疫调节活性则导致长期效应,包括被感染肝细胞的破坏,病毒抗原持续丧失和血清学转换。

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