Zhang Jingwu
Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine, and Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
J Clin Invest. 2007 Apr;117(4):871-3. doi: 10.1172/JCI31860.
IFN-gamma has long been recognized as a signature proinflammatory cytokine that plays a central role in inflammation and autoimmune disease. There is now emerging evidence indicating that IFN-gamma possesses unexpected properties as a master regulator of immune responses and inflammation. In this issue of the JCI, Guillonneau et al. show that indefinite allograft survival induced by CD40Ig treatment is mediated by CD8(+)CD45RC(low) T cells through the production of IFN-gamma (see the related article beginning on page 1096), supporting the emerging view that IFN-gamma is critical in the self-regulation of inflammation. These contradictory roles of IFN-gamma, perhaps best understood by the principle of yin and yang, represent one of nature's paradoxes, whereby the same cytokine functions as an inducer as well as a regulator for inflammation. Understanding this complex process of IFN-gamma signaling is essential, as it has therapeutic implications.
长期以来，γ干扰素一直被认为是一种标志性的促炎细胞因子，在炎症和自身免疫性疾病中起核心作用。现在有新出现的证据表明，γ干扰素作为免疫反应和炎症的主要调节因子具有意想不到的特性。在本期《临床研究杂志》中，吉洛诺等人表明，CD40Ig治疗诱导的同种异体移植物无限期存活是由CD8(+)CD45RC(低)T细胞通过产生γ干扰素介导的（见第1096页开始的相关文章），这支持了γ干扰素在炎症自我调节中至关重要这一新兴观点。γ干扰素的这些矛盾作用，或许用阴阳学说来理解最为恰当，代表了自然界的悖论之一，即同一种细胞因子既作为炎症的诱导剂又作为调节剂发挥作用。理解γ干扰素信号传导的这一复杂过程至关重要，因为它具有治疗意义。
