Division of Rheumatology, Department of Medicine, University of Texas Health Science Center at Houston, 6431 Fannin, Houston, TX 77030, USA.
Expert Rev Clin Immunol. 2011 Jul;7(4):445-8. doi: 10.1586/eci.11.31.
Evaluation of: Avouac J, Fürnrohr BG, Tomcik M et al. Inactivation of the transcription factor STAT-4 prevents inflammation-driven fibrosis in animal models of systemic sclerosis. Arthritis Rheum. 63(3), 800-809 (2011). STAT4 has been identified as a genetic risk factor for the development of autoimmune diseases including systemic sclerosis. STAT4 regulates Th1 cell development and cell-mediated immunity, but it is not known how it may regulate the development of dermal fibrosis. Using the bleomycin-induced dermal fibrosis model, it has now been demonstrated that STAT4-deficient mice have reduced dermal fibrosis in part via STAT4-dependent alterations in T-cell proliferation and cytokine production. These data stress the importance of STAT4 in autoimmune diseases such as systemic sclerosis and provide an important direction for future research to improve our understanding of systemic sclerosis pathogenesis.
Avouac J、Fürnrohr BG、Tomcik M 等人。STAT4 转录因子失活可预防系统性硬化症动物模型中的炎症驱动性纤维化。关节炎与风湿病。63(3)，800-809（2011 年）。STAT4 已被确定为包括系统性硬化症在内的自身免疫性疾病发展的遗传风险因素。STAT4 调节 Th1 细胞的发育和细胞介导的免疫，但尚不清楚它如何调节皮肤纤维化的发展。使用博来霉素诱导的皮肤纤维化模型，现已证明 STAT4 缺陷小鼠的皮肤纤维化减少，部分原因是 STAT4 依赖性 T 细胞增殖和细胞因子产生的改变。这些数据强调了 STAT4 在自身免疫性疾病（如系统性硬化症）中的重要性，并为未来的研究提供了一个重要方向，以提高我们对系统性硬化症发病机制的理解。
