The role of IL-5, IL-6 and IL-10 in primary and vaccine-primed immune responses to infection with Friend retrovirus (Murine leukaemia virus).

The role of IL-5, IL-6 and IL-10 in primary and vaccine-primed immune responses to infection with Friend retrovirus (Murine leukaemia virus).
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IL-5、IL-6 和 IL-10 在针对 Friend 逆转录病毒(鼠白血病病毒)感染的初级免疫反应和疫苗引发的免疫反应中的作用。

DOI:
10.1099/0022-1317-82-6-1349
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发表时间:
2001
期刊:
The Journal of general virology
影响因子:
--
通讯作者:
Dittmer,U
Dittmer,U
中科院分区:
--
文献类型:
--
作者:
Strestik,BD;Olbrich,AR;Hasenkrug,KJ;Dittmer,U

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宿主对病毒感染的防御受到细胞因子的强烈影响。我们研究了B细胞刺激细胞因子IL-5和IL-6以及免疫抑制细胞因子IL-10在小鼠抗Friend逆转录病毒(FV)(鼠白血病病毒)感染的初次和二次免疫应答期间的作用。IL-5−/−小鼠在控制急性FV感染的能力方面与C57 BL/6野生型小鼠相当。相比之下,IL-6−/−和IL-10−/−小鼠脾细胞中的病毒载量显著增加。然而,这种急性FV复制的受损控制并没有改变IL-6−/−和IL-10−/−小鼠对持续性FV的长期控制。在攻击前用活的减毒疫苗病毒免疫保护所有三种类型的精氨酸缺陷小鼠免受高水平的脾病毒,尽管发现接种的IL-5和IL-6缺陷小鼠的病毒中和IgG类抗体的滴度显著降低。结果表明,IL-6和IL-10有助于对FV的初级免疫应答,但在持续感染和疫苗引发的次级应答期间被抑制。
The defence of a host against viral infections is strongly influenced by cytokines. We investigated the role of the B-cell stimulating cytokines IL-5 and IL-6, and the immuno-suppressive cytokine IL-10, during primary and secondary immune responses in mice against infection with Friend retrovirus (FV) (Murine leukaemia virus). IL-5−/−mice were comparable to C57BL/6 wild-type mice in their ability to control acute FV infection. In contrast, IL-6−/−and IL-10−/−mice showed significantly enhanced virus loads in spleen cells. However, this impaired control of acute FV replication did not alter the long-term control over persistent FV in IL-6−/−and IL-10−/−mice. Immunization with a live attenuated vaccine virus prior to challenge protected all three types of cytokine-deficient mice from high levels of spleen virus, despite the finding that the vaccinated IL-5- and IL-6-deficient mice had significantly reduced titres of virus-neutralizing IgG class antibodies. The results indicate that IL-6 and IL-10 contribute to primary immune responses against FV, but are dispensable during persistent infection and vaccine-primed secondary responses.
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