Lee Byunghyuk, Ko Eunhee, Lee Jiyeon, Jo Yuna, Hwang Hyunju, Goh Tae Sik, Joo Myungsoo, Hong Changwan
Department of Anatomy and Cell Biology, Pusan National University School of Medicine.
Division of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan.
Int J Chron Obstruct Pulmon Dis. 2017 Mar 8;12:817-827. doi: 10.2147/COPD.S123405. eCollection 2017.
Cigarette smoking (CS) is a major cause of considerable morbidity and mortality by inducing lung cancer and COPD. COPD, a smoking-related disorder, is closely related to the alteration of immune system and inflammatory processes that are specifically mediated by T cells. Soluble common gamma chain (sγc) has recently been identified as a critical regulator of the development and differentiation of T cells. We examined the effects of sγc in a cigarette smoke extract (CSE) mouse model. The sγc level in CSE mice serum is significantly downregulated, and the cellularity of lymph node (LN) is systemically reduced in the CSE group. Overexpression of sγc enhances the cellularity and IFNγ production of CD8 T cells in LN and also enhances Th1 and Th17 differentiation of CD4 T cells in the respiratory tract. Mechanistically, the downregulation of sγc expression mediated by CSE is required to prevent excessive inflammatory T cell responses. Therefore, our data suggest that sγc may be one of the target molecules for the control of immunopathogenic progresses in COPD.
吸烟是导致肺癌和慢性阻塞性肺疾病（COPD）从而造成相当高发病率和死亡率的主要原因。COPD是一种与吸烟相关的疾病，与免疫系统的改变以及由T细胞特异性介导的炎症过程密切相关。可溶性共同γ链（sγc）最近被确定为T细胞发育和分化的关键调节因子。我们在香烟烟雾提取物（CSE）小鼠模型中研究了sγc的作用。CSE小鼠血清中的sγc水平显著下调，CSE组的淋巴结（LN）细胞数量系统性减少。sγc的过表达增强了LN中CD8 T细胞的细胞数量和IFNγ产生，也增强了呼吸道中CD4 T细胞的Th1和Th17分化。从机制上讲，CSE介导的sγc表达下调是为了防止过度的炎症性T细胞反应。因此，我们的数据表明sγc可能是控制COPD免疫致病进程的靶分子之一。
