Kikodze N, Pantsulaia I, Chikovani T
Tbilisi State Medical University, Institute of Medical Biotechnology, Georgia.
Georgian Med News. 2016 Dec(261):62-68.
Chronic inflammation of joints of autoimmune origin - rheumatoid arthritis - develops due to deplorable coincidence of genetic, immune and environmental factors. Th17 cells are considered as the main effector cells in the pathogenesis of rheumatoid arthritis. Analysis of many reports clarify positive correlation between the frequencies of circulating Th17 cells, serum levels of IL-17A and IL-23, synovial IL-17 and disease activity. Autoreactive Th clone response is regulated by the certain population of suppressor cells - T regulatory cells (Tregs). Contradictory results have been reported concerning Treg cell proportion in RA peripheral blood, but there is a general agreement on Treg cell enrichment in RA synovial fluid, that somehow compensates inflammation, but cytokine environment in the inflamed joint reduces functional activity of Tregs. Imbalance between Th17 and Treg cells may play a initiative role in RA pathogenesis because predominant Th17 cells can provoke vigorous pro-inflammatory response by producing IL-17 and impaired Tregs, partly due to the cytokine microenvironment, cannot regulate autoreactive immune response. Currently, a major focus of study in RA is to control IL-17 and modulate Treg activity in order to design new and improved therapies to limit inflammation and re-establish self-tolerance.
自身免疫性起源的关节慢性炎症——类风湿关节炎——是由于遗传、免疫和环境因素的不幸巧合而发展起来的。Th17细胞被认为是类风湿关节炎发病机制中的主要效应细胞。对许多报告的分析表明，循环Th17细胞频率、血清IL-17A和IL-23水平、滑膜IL-17与疾病活动之间存在正相关。自身反应性Th克隆反应受特定抑制细胞群——调节性T细胞（Tregs）的调节。关于RA外周血中Treg细胞比例的报道结果相互矛盾，但对于RA滑液中Treg细胞富集存在普遍共识，即Treg细胞在一定程度上可补偿炎症，但炎症关节中的细胞因子环境会降低Tregs的功能活性。Th17和Treg细胞之间的失衡可能在RA发病机制中起主导作用，因为占主导地位的Th17细胞可通过产生IL-17引发强烈的促炎反应，而受损的Tregs（部分由于细胞因子微环境）无法调节自身反应性免疫反应。目前，RA研究的一个主要重点是控制IL-17并调节Treg活性，以便设计新的和改进的疗法来限制炎症并重建自身耐受性。
