Procaccini Claudio, Pucino Valentina, De Rosa Veronica, Marone Gianni, Matarese Giuseppe
Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche , Napoli , Italy.
Dipartimento di Scienze Mediche Traslazionali, Università di Napoli "Federico II" , Napoli , Italy.
Front Immunol. 2014 Apr 7;5:143. doi: 10.3389/fimmu.2014.00143. eCollection 2014.
The nervous and immune systems have long been considered as compartments that perform separate and different functions. However, recent clinical, epidemiological, and experimental data have suggested that the pathogenesis of several immune-mediated disorders, such as multiple sclerosis (MS), might involve factors, hormones, and neural mediators that link the immune and nervous system. These molecules are members of the same superfamily, which allow the mutual and bi-directional neural-immune interaction. More recently, the discovery of leptin, one of the most abundant adipocyte-derived hormones that control food intake and metabolism, has suggested that nutritional/metabolic status, acting at central level, can control immune self-tolerance, since it promotes experimental autoimmune encephalomyelitis, an animal model of MS. Here, we summarize the most recent advances and the key players linking the central nervous system, immune tolerance, and the metabolic status. Understanding this coordinated interaction may pave the way for novel therapeutic approaches to increase host defense and suppress immune-mediated disorders.
长期以来，神经系统和免疫系统一直被视为执行各自不同功能的独立部分。然而，最近的临床、流行病学和实验数据表明，几种免疫介导疾病（如多发性硬化症，MS）的发病机制可能涉及连接免疫系统和神经系统的因子、激素及神经介质。这些分子属于同一超家族成员，使得神经 - 免疫之间能够相互及双向作用。最近，瘦素（一种控制食物摄入和新陈代谢的最丰富的脂肪细胞衍生激素）的发现表明，在中枢水平起作用的营养/代谢状态可以控制免疫自我耐受，因为它会促进实验性自身免疫性脑脊髓炎（一种MS的动物模型）。在此，我们总结了连接中枢神经系统、免疫耐受和代谢状态的最新进展及关键因素。了解这种协同相互作用可能为增加宿主防御和抑制免疫介导疾病的新治疗方法铺平道路。
