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麻疹病毒对T细胞功能的免疫抑制作用——体外未影响白细胞介素-2释放或细胞毒性T细胞活性

The immunosuppressive effects of measles virus on T cell function--failure to affect IL-2 release or cytotoxic T cell activity in vitro.

作者信息

Borysiewicz L K, Casali P, Rogers B, Morris S, Sissons J G

出版信息

Clin Exp Immunol. 1985 Jan;59(1):29-36.

Abstract

Measles virus (MV) is known to depress T cell function. In order to determine whether this results from alteration in the production of, or response to, interleukin-2 (IL-2) we studied the effect of in vitro infection with MV on human IL-2 dependent T cell lines. MV produced a cytopathic productive infection in these cells. Class I allospecific cytotoxic T cells retained their cytotoxic activity 48 h after infection. Both cytotoxic and Leu 3a/4a positive T cell lines continued to respond to IL-2 by proliferation up to 26 h after infection. The ability of human tonsillar lymphocytes to generate IL-2 in response to phytohaemagglutinin following MV infection was then studied. In early measles infection (up to 48 h) there was no suppression of IL-2 production: in fact measles infected cells spontaneously released low levels of IL-2 in the absence of lectin. Similarly, IL-2 release was not affected by Herpes simplex virus infection of such cultures, although lymphocytes infected with Sendai or respiratory syncytial viruses produced considerably less IL-2. These observations suggest that MV-induced immunosuppression is not a result of inhibition of differentiated T cell function, IL-2 generation or responsiveness, but may be more directly related to virus-induced cytopathic effects in activated T cells.

摘要

已知麻疹病毒(MV)会抑制T细胞功能。为了确定这是否是由于白细胞介素-2(IL-2)产生的改变或对其反应的改变所致,我们研究了体外感染MV对人IL-2依赖性T细胞系的影响。MV在这些细胞中产生了细胞病变性增殖性感染。I类同种异体特异性细胞毒性T细胞在感染后48小时仍保留其细胞毒性活性。细胞毒性T细胞系和Leu 3a/4a阳性T细胞系在感染后长达26小时内继续通过增殖对IL-2作出反应。随后研究了人扁桃体淋巴细胞在感染MV后对植物血凝素产生IL-2的能力。在麻疹早期感染(长达48小时)中,IL-2的产生没有受到抑制:事实上,在没有凝集素的情况下,感染麻疹的细胞会自发释放低水平的IL-2。同样,单纯疱疹病毒感染此类培养物对IL-2的释放没有影响,尽管感染仙台病毒或呼吸道合胞病毒的淋巴细胞产生的IL-2要少得多。这些观察结果表明,MV诱导的免疫抑制不是分化的T细胞功能、IL-2产生或反应性受到抑制的结果,而可能更直接地与病毒诱导的活化T细胞的细胞病变效应有关。

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