首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells.
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Interleukin-1 receptor antagonist suppresses experimental autoimmune encephalomyelitis (EAE) in rats by influencing the activation and proliferation of encephalitogenic cells.

机译:白介素-1受体拮抗剂通过影响致脑原性细胞的活化和增殖来抑制大鼠实验性自身免疫性脑脊髓炎(EAE)。

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Considering the role of pleiotropic interleukin-1 (IL-1) in inflammation and autoimmunity, studies were designed to examine whether specific blockade of IL-1 may influence these processes in the CNS. Although the role of CD4+ T cells in eliciting clinical signs of experimental autoimmune encephalomyelitis (EAE) has been unequivocally demonstrated, the exact mechanism by which encephalitogenic cells initiate disease process and bring about clinical signs still remains to be defined. We have evaluated the effect of human recombinant interleukin-1 receptor antagonist (IL-1Ra) in vivo on the course of actively induced EAE in highly susceptible Dark Agouti (DA) rats. The rats which were treated during the induction phase of disease (days 0-6) with IL-1Ra (350 microg/rat/day) developed milder signs of EAE, when compared to saline-treated control animals immunized with encephalitogen, which developed severe single episode disease. The transfer of lymph node cells (LNC) isolated from MBP-primed DA rats and stimulated in vitro with MBP and ConA to naive syngeneic animals resulted in the development of EAE in all recipients. However, rats injected with LNC that have been stimulated in vitro in the presence of IL-1Ra (10 microg/ml) developed significantly milder disease. Diminished encephalitogenic capacity of LNC correlated with lower proliferative response to antigen and mitogen and decreased expression of IL-2 receptors. These data provide further evidence that IL-1 is an important factor for activation of EAE inducing T lymphocytes.
机译:考虑到多效性白介素-1(IL-1)在炎症和自身免疫中的作用,设计了研究以检查IL-1的特异性阻断是否可能影响中枢神经系统的这些过程。尽管已经明确证明了CD4 + T细胞在引发实验性自身免疫性脑脊髓炎(EAE)的临床体征中的作用,但致脑炎细胞引发疾病过程并产生临床体征的确切机制仍有待确定。我们已经评估了人类重组白介素-1受体拮抗剂(IL-1Ra)在体内对高度敏感的黑暗刺槐(DA)大鼠中主动诱导的EAE的作用。与用脑源原免疫的盐水处理对照组动物相比,在疾病诱导阶段(0-6天)用IL-1Ra(350微克/大鼠/天)治疗的大鼠出现了较轻的EAE体征。单发疾病。从MBP引发的DA大鼠中分离并用MBP和ConA体外刺激的淋巴结细胞(LNC)转移到幼稚的同系动物中,导致所有受体EAE的发展。但是,注射有LNC的大鼠在存在IL-1Ra(10 microg / ml)的情况下在体外受到刺激,其病情明显减轻。 LNC的致脑病能力降低与对抗原和有丝分裂原的增殖反应降低以及IL-2受体表达降低有关。这些数据提供了进一步的证据,证明IL-1是激活EAE诱导T淋巴细胞的重要因素。

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