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首页> 外文期刊>Infection and immunity >Protective effect of a T-cell-dependent immunosuppressive, B-cell-mitogenic protein (F3'EP-Si, or P90) produced by Streptococcus intermedius.
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Protective effect of a T-cell-dependent immunosuppressive, B-cell-mitogenic protein (F3'EP-Si, or P90) produced by Streptococcus intermedius.

机译：中间链球菌产生的T细胞依赖性免疫抑制，B细胞有丝分裂蛋白（F3'EP-Si或P90）的保护作用。

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The role of a previously described bacterial protein (F3'EP-Si), now designated P90, in the survival of Streptococcus intermedius in the host was investigated, and the immunosuppressive and B-cell-mitogenic effects of this protein were further characterized. C57BL6 mice treated with P90 were about 50 times more susceptible to infection with this bacterium than untreated mice. One of seven splenocytes of C57BL/6 mice were activated by P90. Marked splenomegaly was observed in mice treated with P90, with increased numbers of splenic mononuclear cells and polyclonal immunoglobulin-secreting plaque-forming cells. Peak responses were seen on day 3 for immunoglobulin M (IgM) and on day 5 for IgG, with an isotypic pattern consisting predominantly of IgG2a and IgG2b. When mice were treated with P90 before being primed with sheep erythrocytes, polyclonal immunoglobulin synthesis was accompanied by an ephemeral stimulation of the specific immune response against sheep erythrocytes that was quickly replaced by a dramatic immunosuppression. In contrast, when mice were treated with P90 after being primed, the polyclonal activation was comparatively much less evident and there was no suppression of the specific immune response. Immunosuppression was considerably reduced in mice thymectomized as adults or depleted of CD8+ cells. Adoptive transfer experiments showed that B cells obtained from P90-treated mice were less able to respond to an antigenic challenge, even in the presence of normal T cells, and that T cells obtained from P90-treated mice could actively suppress the specific immune response of normal B cells.
机译：研究了先前描述的细菌蛋白（F3'EP-Si）（现在命名为P90）在中间链球菌在宿主中的存活中的作用，并进一步表征了该蛋白的免疫抑制和B细胞有丝分裂作用。用P90处理的C57BL6小鼠对这种细菌的感染敏感性是未处理小鼠的50倍。 C90BL / 6小鼠的七个脾细胞之一被P90激活。在用P90处理的小鼠中观察到明显的脾肿大，脾单核细胞和分泌多克隆免疫球蛋白的噬菌斑形成细胞数量增加。免疫球蛋白M（IgM）在第3天和IgG在第5天出现峰响应，其同型模式主要由IgG2a和IgG2b组成。当在用绵羊红细胞引发小鼠之前用P90治疗小鼠时，多克隆免疫球蛋白的合成伴随着短暂的针对绵羊红细胞的特异性免疫反应的刺激，该刺激迅速被戏剧性的免疫抑制所取代。相反，当小鼠在初免后用P90治疗时，多克隆激活相对不那么明显，并且没有抑制特异性免疫应答。在成年或无CD8 +细胞的胸腺切除小鼠中，免疫抑制显着降低。过继转移实验表明，即使在正常T细胞存在的情况下，从接受P90治疗的小鼠获得的B细胞对抗原性攻击的反应也较弱，并且从接受P90治疗的小鼠获得的T细胞可以积极抑制小鼠的特异性免疫应答。正常的B细胞。

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