Woo P
Windeyer Institute, University College London, United Kingdom.
Baillieres Clin Rheumatol. 1998 May;12(2):219-28. doi: 10.1016/s0950-3579(98)80016-2.
Cytokines are important mediators of the immune response as well as the inflammatory response. Those concerned primarily with cell growth, differentiation and activation of cells within the immune system are called interleukins, of which there are now 18. Exposure to antigenic and environmental stimuli causes T cells to differentiate and polarise into Th1 or 2-like cells with different cytokine profiles, and requiring different cytokines for differentiation (IL-12 for Th1 and IL-4 for Th2). Homeostasis is usually restored as these cells are mutually inhibitory. Autoimmune diseases have been associated with a persistent imbalance with more Th1-like cells, which are thought to contribute to pathology. With regard to juvenile chronic arthritis (JCA), there is some preliminary evidence of this imbalance in the oligoarticular subgroup. Imbalance of pro-inflammatory cytokines, IL-1 and TNF with their natural inhibitors has also been shown to contribute to persistence of inflammation. In the case of JCA, there has been some evidence that these imbalances could account for some of the disease phenotypes. Furthermore, the tendency to imbalance is genetically determined.
细胞因子是免疫反应以及炎症反应的重要介质。那些主要与免疫系统内细胞的生长、分化和激活有关的细胞因子被称为白细胞介素,目前已知的有18种。暴露于抗原和环境刺激会导致T细胞分化并极化成为具有不同细胞因子谱的Th1或Th2样细胞,且分化需要不同的细胞因子(Th1分化需要IL-12,Th2分化需要IL-4)。由于这些细胞相互抑制,通常可恢复内环境稳态。自身免疫性疾病与更多Th1样细胞的持续失衡有关,这些细胞被认为会导致病理变化。关于青少年慢性关节炎(JCA),在少关节亚组中有一些这种失衡的初步证据。促炎细胞因子IL-1和TNF与其天然抑制剂之间的失衡也已被证明会导致炎症持续存在。就JCA而言,有证据表明这些失衡可能是某些疾病表型的原因。此外,失衡的倾向是由基因决定的。