| First Author | Lee B | Year | 2017 |
| Journal | Int J Chron Obstruct Pulmon Dis | Volume | 12 |
| Pages | 817-827 | PubMed ID | 28331303 |
| Mgi Jnum | J:319247 | Mgi Id | MGI:6863323 |
| Doi | 10.2147/COPD.S123405 | Citation | Lee B, et al. (2017) Soluble common gamma chain exacerbates COPD progress through the regulation of inflammatory T cell response in mice. Int J Chron Obstruct Pulmon Dis 12:817-827 |
| abstractText | 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 (sgammac) has recently been identified as a critical regulator of the development and differentiation of T cells. We examined the effects of sgammac in a cigarette smoke extract (CSE) mouse model. The sgammac level in CSE mice serum is significantly downregulated, and the cellularity of lymph node (LN) is systemically reduced in the CSE group. Overexpression of sgammac enhances the cellularity and IFNgamma 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 sgammac expression mediated by CSE is required to prevent excessive inflammatory T cell responses. Therefore, our data suggest that sgammac may be one of the target molecules for the control of immunopathogenic progresses in COPD. |
