A Toxoplasma gondii-derived factor(s) stimulates immune downregulation: an in vitro model.

A Toxoplasma gondii-derived factor(s) stimulates immune downregulation: an in vitro model.
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弓形虫衍生因子刺激免疫下调:体外模型。

DOI:
10.1128/iai.63.9.3442-3447.1995
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发表时间:
1995
影响因子:
3.1
通讯作者:
Kasper,LH
Kasper,LH
中科院分区:
医学2区
文献类型:
--
作者:
Haque,S;Haque,A;Kasper,LH

文献摘要

相似文献

在体内感染弓形虫后,已观察到T细胞淋巴增殖反应的抑制和白细胞介素2(IL-2)产生的下调。在本研究中,开发了一种实验性体外小鼠系统,以评估这些反应的动力学。用伴刀豆球蛋白A或抗CD 3单克隆抗体刺激未感染小鼠的正常脾细胞,并与弓形虫速殖子直接或通过transwell分离共培养。随着培养物中寄生虫浓度的增加,观察到淋巴增殖反应的逐步下降。无论是热杀死或甲醛固定的寄生虫刺激这种下调反应的脾细胞。IL-2产生的下降与淋巴细胞增殖的减少有关。向培养上清液中加入IL-10抗体或热灭活抗弓形虫血清可部分中和对淋巴细胞增殖的抑制作用。应答者脾细胞的细胞因子分析表明IL-2和IL-2受体的信息减少,IL-10增加。总之,这些观察结果表明,在鼠系统中的体外培养期间,表达了刺激可溶性因子(如IL-10)释放的寄生虫抗原,所述可溶性因子抑制有丝分裂原刺激的T细胞的增殖。
Suppression of the T-cell lymphoproliferative response and downregulation of interleukin 2 (IL-2) production by Toxoplasma gondii has been observed following in vivo infection. In this study, an experimental in vitro murine system was developed to evaluate the kinetics of these responses. Normal splenocytes from uninfected mice were stimulated with either concanavalin A or an anti-CD3 monoclonal antibody and cocultured with Toxoplasma tachyzoites either directly or separated by a transwell. A progressive decline in the lymphoproliferative response was observed as the concentration of parasites in culture increased. Neither heat-killed nor formaldehyde-fixed parasites stimulated this downregulatory response by the splenocytes. A decline in IL-2 production was associated with the decrease in lymphocyte proliferation. The addition of an antibody to IL-10 or heat-inactivated anti-Toxoplasma sera to the culture supernatant partially neutralized the inhibitory effect on lymphocyte proliferation. Cytokine analysis of the responder splenocytes demonstrated a decrease in the message for IL-2 and IL-2 receptor and an increase in IL-10. Together, these observations suggest that during in vitro culture in a murine system, parasite antigens that stimulate the release of a soluble factor(s), such as IL-10, that inhibits proliferation of mitogen-stimulated T cells are expressed.