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。
Autoantigen specific IL-2 activated CD4CD25T regulatory cells inhibit induction of experimental autoimmune neuritis.
机构信息
Immune Tolerance Laboratory, Faculty of Medicine, UNSW Sydney, Ingham Institute, Liverpool, NSW, Australia.
Immune Tolerance Laboratory, Faculty of Medicine, UNSW Sydney, Ingham Institute, Liverpool, NSW, Australia; Departments of Neurology Liverpool Health Service, Liverpool, NSW, Australia.
出版信息
J Neuroimmunol. 2020 Apr 15;341:577186. doi: 10.1016/j.jneuroim.2020.577186. Epub 2020 Feb 3.
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 CD4CD25T cells both from sensitized hosts or from naïve hosts after ex-vivo activation by PNM and rIL-2. Transfer of naïve CD4CD25T cells has no effect on EAN, nor did naïve CD4CD25T cells activated with rIL-2 and renal tubular antigen. Culture of naive CD4CD25Treg with rIL-2 and PNM induced mRNA for the IFN-gamma receptor. We showed naïve CD4CD25T cells activated by specific auto-antigen and rIL-2 produced more potent antigen-specific Treg that may have therapeutic potential.
实验性自身免疫性神经炎 (EAN) 由周围神经髓鞘 (PNM) 诱导，具有自限性，用 PNM 再次免疫不会重新激活疾病。本研究显示，PNM 和 rIL-2 体外激活后，来自致敏宿主或来自幼稚宿主的 CD4CD25T 细胞均可抑制 EAN。幼稚 CD4CD25T 细胞转移对 EAN 没有影响，rIL-2 和肾小管抗原激活的幼稚 CD4CD25T 细胞也没有影响。rIL-2 和 PNM 培养的幼稚 CD4CD25Treg 诱导 IFN-γ受体的 mRNA。我们表明，由特异性自身抗原和 rIL-2 激活的幼稚 CD4CD25T 细胞产生了更有效的抗原特异性 Treg，可能具有治疗潜力。
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