Theofilopoulos A N, Koundouris S, Kono D H, Lawson B R
The Scripps Research Institute, Department of Immunology/IMM3, La Jolla, CA 92037, USA.
Arthritis Res. 2001;3(3):136-41. doi: 10.1186/ar290. Epub 2001 Feb 14.
The classification of T helper cells into type 1 (Th1) and type 2 (Th2) led to the hypothesis that Th1 cells and their cytokines (interleukin [IL]-2, interferon [IFN]-gamma) are involved in cell-mediated autoimmune diseases, and that Th2 cells and their cytokines (IL-4, IL-5, IL-10, IL-13) are involved in autoantibody(humoral)-mediated autoimmune diseases. However, this paradigm has been refuted by recent studies in several induced and spontaneous mouse models of systemic lupus erythematosus, which showed that IFN-gamma is a major effector molecule in this disease. These and additional findings, reviewed here, suggest that these two cross-talking classes of cytokines can exert autoimmune disease-promoting or disease-inhibiting effects without predictability or strict adherence to the Th1-versus-Th2 dualism.
辅助性T细胞被分为1型（Th1）和2型（Th2），由此产生了一种假说，即Th1细胞及其细胞因子（白细胞介素[IL]-2、干扰素[IFN]-γ）参与细胞介导的自身免疫性疾病，而Th2细胞及其细胞因子（IL-4、IL-5、IL-10、IL-13）参与自身抗体（体液）介导的自身免疫性疾病。然而，最近在几种诱导性和自发性系统性红斑狼疮小鼠模型中的研究反驳了这一范式，这些研究表明IFN-γ是这种疾病的主要效应分子。本文所综述的这些及其他发现表明，这两类相互作用的细胞因子可以发挥促进自身免疫性疾病或抑制疾病的作用，而无法预测或严格遵循Th1与Th2的二元论。
