Biswas Partha S, Kang Kyuho, Gupta Sanjay, Bhagat Govind, Pernis Alessandra B
Autoimmunity & Inflammation Program, Hospital for Special Surgery, New York, NY, USA.
Methods Mol Biol. 2012;900:233-51. doi: 10.1007/978-1-60761-720-4_11.
T-helper cell 17 (Th17) cells play an important role in the pathogenesis of many autoimmune disorders including Rheumatoid Arthritis (RA) and Systemic Lupus Erythematosus (SLE). In this chapter we describe a murine model where deregulated production of IL-17 and IL-21 can lead to either lupus-like disease or RA-like symptoms depending on the genetic background. We delineate the key techniques that can be used to dissect the mechanisms responsible for the pathogenesis of these diseases at both a cellular and molecular level including in vitro Th17 cell differentiation, chromatin immunoprecipitation assays, and retroviral transduction experiments. We also describe the methodologies that can be utilized to monitor the classic clinical findings of RA and SLE in murine models. Given the broad involvement of deregulated production of IL-17 and IL-21 in autoimmunity, many of these techniques could also be valuable for the investigation of these pathways in murine models of other autoimmune diseases.
辅助性T细胞17（Th17）细胞在包括类风湿性关节炎（RA）和系统性红斑狼疮（SLE）在内的许多自身免疫性疾病的发病机制中发挥着重要作用。在本章中，我们描述了一种小鼠模型，其中IL-17和IL-21的失控产生可导致狼疮样疾病或RA样症状，具体取决于遗传背景。我们阐述了可用于在细胞和分子水平剖析这些疾病发病机制的关键技术，包括体外Th17细胞分化、染色质免疫沉淀测定和逆转录病毒转导实验。我们还描述了可用于监测小鼠模型中RA和SLE经典临床发现的方法。鉴于IL-17和IL-21失控产生在自身免疫中的广泛参与，许多这些技术对于研究其他自身免疫性疾病小鼠模型中的这些途径也可能具有价值。
