Kostic Milos, Stojanovic Ivana, Marjanovic Goran, Zivkovic Nikola, Cvetanovic Ana
Department of Immunology, Medical Faculty, University of Nis, Blvd. Dr. Zorana Djindjica 81, 18000 Nis, Serbia.
Department of Biochemistry, Medical Faculty, University of Nis, Blvd. Dr. Zorana Djindjica 81, 18000 Nis, Serbia.
Cell Immunol. 2015 Aug;296(2):122-32. doi: 10.1016/j.cellimm.2015.04.006. Epub 2015 Apr 28.
Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disorder of central nervous system, in which myelin specific CD4(+) T cells have a central role in orchestrating pathological events involved in disease pathogenesis. There is compelling evidence that Th1, Th9 and Th17 cells, separately or in cooperation, could mediate deleterious autoimmune response in MS. However, the phenotype differences between Th cell subpopulations initially employed in MS pathogenesis are mainly reflected in the different patterns of inflammation introduction, which results in the development of characteristic pathological features (blood-brain barrier disruption, demyelination and neurodegeneration), clinically presented with MS symptoms. Although, autoimmunity was traditionally seen as deleterious, some studies indicated that autoimmunity mediated by Th2 cells and T regulatory cells could be protective by nature. The concept of protective autoimmunity in MS pathogenesis is still poorly understood, but could be of great importance in better understanding of MS immunology and therefore, creating better therapeutic strategies.
多发性硬化症（MS）是一种中枢神经系统的慢性炎症性和神经退行性疾病，其中髓鞘特异性CD4(+) T细胞在协调疾病发病机制中涉及的病理事件方面发挥核心作用。有确凿证据表明，Th1、Th9和Th17细胞单独或协同作用，可在MS中介导有害的自身免疫反应。然而，最初参与MS发病机制的Th细胞亚群之间的表型差异主要体现在炎症引发的不同模式上，这导致了特征性病理特征（血脑屏障破坏、脱髓鞘和神经变性）的发展，临床上表现为MS症状。尽管传统上认为自身免疫是有害的，但一些研究表明，由Th2细胞和T调节细胞介导的自身免疫本质上可能具有保护作用。MS发病机制中保护性自身免疫的概念仍知之甚少，但对于更好地理解MS免疫学以及因此制定更好的治疗策略可能非常重要。
