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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Discontinuation of treatment with IFN-beta leads to exacerbation of experimental autoimmune encephalomyelitis in Lewis rats. Rapid reversal of the antiproliferative activity of IFN-beta and excessive expansion of autoreactive T cells as disease promo
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Discontinuation of treatment with IFN-beta leads to exacerbation of experimental autoimmune encephalomyelitis in Lewis rats. Rapid reversal of the antiproliferative activity of IFN-beta and excessive expansion of autoreactive T cells as disease promo

机译：中断使用IFN-β治疗可导致Lewis大鼠实验性自身免疫性脑脊髓炎恶化。快速逆转IFN-β的抗增殖活性和自身反应性T细胞的过度扩增

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IFN-beta has recently been shown to exert remarkable beneficial effects on disease development in patients with early stage relapsing-remitting MS. The specific immune mechanism(s) by which IFN-beta ameliorates this human demyelinating disease is at present undefined. One potential mechanism may reside in the antiproliferative activity of IFN-beta which may inhibit the expansion of autoaggressive T cells thereby limiting disease progression. In the present study we investigated whether the administration of recombinant rat IFN-beta (rrIFN-beta) to Lewis rats with actively induced experimental autoimmune encephalomyelitis (EAE) inhibits the expansion of encephalitogenic T cells in lymphoid organs and as such may contribute to suppression of disease activity in this widely used animal model for MS. Our data show that daily administrations of > or = 3 x 10(5) u rrIFN-beta to EAE rats, starting two days before MBP sensitization and continued for 10 days led to a dramatic and dose-dependent reduction in encephalitogenic T cells in both spleen and inguinal lymph nodes at day 8 post-immunization (p.i.). However, the rrIFN-beta-mediated reduction in effector T cells did not ameliorate paralytic disease as expected but significantly enhanced the severity of EAE. Analyses of lymphoid organs in the remission phase of EAE revealed strongly elevated numbers of encephalitogenic T cells in rrIFN-beta-treated versus control rats suggesting a rapid reversal of the antiproliferative action of rrIFN-beta followed by an overshoot in the subsequent expansion of these effector T cells. In conformity with higher numbers of encephalitogenic T cells and worsening of disease, animals also showed significantly greater perivascular inflammation in the CNS. The relevance of our findings in relation to the beneficial effects of IFN-beta in MS is discussed.
机译：最近显示，IFN-β对早期复发-缓解型MS患者的疾病发展具有显着的有益作用。目前尚不清楚IFN-β改善人脱髓鞘疾病的特异性免疫机制。一种潜在的机制可能在于IFN-β的抗增殖活性，它可能抑制自激性T细胞的扩增，从而限制了疾病的进展。在本研究中，我们调查了向积极诱导的实验性自身免疫性脑脊髓炎（EAE）的Lewis大鼠给药重组大鼠IFN-beta（rrIFN-beta）是否能抑制淋巴器官中致脑性T细胞的扩增，从而可能有助于抑制这种在MS中广泛使用的动物模型中的疾病活性。我们的数据表明，MBE致敏前两天开始每天向EAE大鼠给药>或= 3 x 10（5）u rrIFN-beta，持续10天导致这两种情况中致脑病性T细胞的显着和剂量依赖性降低免疫后第8天（pi）的脾脏和腹股沟淋巴结。然而，rrIFN-β介导的效应T细胞减少并未如预期的那样改善麻痹性疾病，但显着增强了EAE的严重性。对EAE缓解期的淋巴器官的分析表明，与对照大鼠相比，在用rrIFN-beta治疗的大鼠中，致脑病性T细胞的数量大大增加，表明rrIFN-beta的抗增殖作用迅速逆转，随后这些效应子的扩展过高T细胞。与脑致病性T细胞数量增多和疾病恶化相一致，动物在中枢神经系统中还表现出明显更大的血管周围炎症。讨论了我们的发现与IFN-β在MS中的有益作用的相关性。

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