Stübgen Joerg-Patrick
Department of Neurology and Neuroscience, Weill Medical College of Cornell University/New York Presbyterian Hospital, New York, NY 10065-4885, USA.
J Neuroimmunol. 2009 Jul 25;212(1-2):132-41. doi: 10.1016/j.jneuroim.2009.04.015. Epub 2009 May 13.
Interferon-beta (IFNbeta) is an extra-cellular protein mediator of host defense and homeostasis. IFNbeta has well-established direct antiviral, antiproliferative and immunomodulatory properties. Recombinant IFNbeta is approved for the treatment of relapsing-remitting multiple sclerosis. The immunomodulatory effects of IFNbeta administration failed to demonstrate consistent benefit during treatment of various autoimmune neuromuscular diseases. Existing studies were flawed due to the often uncontrolled and unblinded nature of protocols, small patient numbers per study, the undetermined optimum dose and schedule of IFNbeta therapy, and the relatively brief periods of IFNbeta administration and clinical follow-up for mostly chronic inflammatory disorders. Additional, controlled, prospective studies are needed to definitely establish the full potential of this cytokine for this group of diseases. IFNbeta therapy may trigger autoantibody production, but only rarely clinically overt autoimmune disease. Anecdotal reports hint at the exceptional association between IFNbeta treatment and the induction or exacerbation of a variety of immune-mediated neuromuscular diseases, likely in genetically predisposed individuals. Thus, recombinant IFNbeta has the theoretical potential to either treat or cause autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks.
β-干扰素(IFNβ)是宿主防御和内环境稳定的一种细胞外蛋白介质。IFNβ具有公认的直接抗病毒、抗增殖和免疫调节特性。重组IFNβ已被批准用于治疗复发缓解型多发性硬化症。在各种自身免疫性神经肌肉疾病的治疗过程中,给予IFNβ的免疫调节作用未能显示出持续的益处。现有研究存在缺陷,原因在于方案往往缺乏对照且未设盲、每项研究的患者数量少、IFNβ治疗的最佳剂量和疗程未确定,以及对于大多数慢性炎症性疾病,IFNβ给药和临床随访时间相对较短。需要进行更多对照的前瞻性研究,以明确确定这种细胞因子在这类疾病中的全部潜力。IFNβ治疗可能引发自身抗体产生,但临床上很少出现明显的自身免疫性疾病。轶事报道提示IFNβ治疗与多种免疫介导的神经肌肉疾病的诱发或加重之间存在特殊关联,可能发生在具有遗传易感性的个体中。因此,重组IFNβ具有通过改变免疫系统网络内复杂而微妙的平衡来治疗或引发自身免疫性神经肌肉疾病的理论潜力。