Experimental autoimmune neuritis (EAN) induced by peripheral nerve myelin (PNM) is self-limiting and re-immunization with PNM does not re-activate disease. This study showed inhibition of EAN by CD4+CD25+T cells both from sensitized hosts or from naïve hosts after ex-vivo activation by PNM and rIL-2. Transfer of naïve CD4+CD25+T cells has no effect on EAN, nor did naïve CD4+CD25+T cells activated with rIL-2 and renal tubular antigen. Culture of naive CD4+CD25+Treg with rIL-2 and PNM induced mRNA for the IFN-gamma receptor. We showed naïve CD4+CD25+T cells activated by specific auto-antigen and rIL-2 produced more potent antigen-specific Treg that may have therapeutic potential.

中文翻译：

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自身抗原特异性 IL-2 激活的 CD4+CD25+T 调节细胞抑制实验性自身免疫性神经炎的诱导

由周围神经髓鞘 (PNM) 诱导的实验性自身免疫性神经炎 (EAN) 是自限性的，用 PNM 重新免疫不会重新激活疾病。该研究表明，在 PNM 和 rIL-2 离体激活后，来自致敏宿主或幼稚宿主的 CD4+CD25+T 细胞对 EAN 的抑制作用。初始 CD4+CD25+T 细胞的转移对 EAN 没有影响，用 rIL-2 和肾小管抗原激活的初始 CD4+CD25+T 细胞也没有影响。幼稚 CD4+CD25+Treg 与 rIL-2 和 PNM 的培养诱导了 IFN-γ 受体的 mRNA。我们展示了被特异性自身抗原激活的幼稚 CD4+CD25+T 细胞，而 rIL-2 产生了可能具有治疗潜力的更有效的抗原特异性 Treg。