Safarzadeh Elham, Jadidi-Niaragh Farhad, Motallebnezhad Morteza, Yousefi Mehdi
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Inflamm Res. 2016 Jul;65(7):511-20. doi: 10.1007/s00011-016-0936-z. Epub 2016 Mar 9.
Multiple sclerosis (MS) is a heterogeneous neurological disorder with multifactorial etiologies characterized by demyelination, axonal degeneration, and oligodendroglial death. It is believed that both genetics and environmental risk factors such as infection are involved in disease etiology. Accumulating evidence indicates that alteration in purinergic system signaling is involved in immunity and inflammation. Adenosine, a key purine nucleoside, has been shown to be produced during metabolic stress, including ischemia, inflammatory condition, and tissue injury.
Extracellular adenosine directly affects various physiological and pathological processes of MS by stimulating G protein-coupled adenosine receptors A1, A2A, A2B, and A3 on the surface of immune cells. It has been suggested that promotion of adenosinergic system may be an important factor in MS pathophysiology and considered as promising therapeutic target for this disease.
In this review, we will discuss about the immunopathologic effects of adenosine on MS and its animal model, experimental autoimmune encephalomyelitis.
多发性硬化症（MS）是一种异质性神经疾病，病因多因素，其特征为脱髓鞘、轴突变性和少突胶质细胞死亡。人们认为遗传因素和诸如感染等环境风险因素均参与疾病病因。越来越多的证据表明嘌呤能系统信号改变参与免疫和炎症过程。腺苷作为关键的嘌呤核苷，已证实在包括缺血、炎症状态和组织损伤等代谢应激期间产生。
细胞外腺苷通过刺激免疫细胞表面的G蛋白偶联腺苷受体A1、A2A、A2B和A3，直接影响MS的各种生理和病理过程。有人提出促进腺苷能系统可能是MS病理生理学中的一个重要因素，并被视为该疾病有前景的治疗靶点。
在本综述中，我们将讨论腺苷对MS及其动物模型实验性自身免疫性脑脊髓炎的免疫病理效应。
