Pasquinelli Virginia, Townsend James C, Jurado Javier O, Alvarez Ivana B, Quiroga María F, Barnes Peter F, Samten Buka, García Verónica E
Department of Biological Chemistry, School of Sciences, University of Buenos Aires, Buenos Aires, Argentina.
J Infect Dis. 2009 Mar 1;199(5):661-5. doi: 10.1086/596742.
Interferon-gamma (IFN-gamma) is crucial for protection against Mycobacterium tuberculosis, and the transcription factor cAMP response element binding protein (CREB) increases IFN-gamma transcription. We determined whether the transmembrane receptor signaling lymphocyte activation molecule (SLAM) and interleukin-17 (IL-17) affect CREB phosphorylation and IFN-gamma production in persons with tuberculosis. When T cells from patients with tuberculosis were activated with M. tuberculosis, 80% of SLAM(+) T cells expressed phosphorylated CREB, and SLAM activation increased CREB phosphorylation and IFN-gamma production. In contrast, IL-17 down-regulated SLAM expression, CREB phosphorylation, and IFN-gamma production. Therefore, IL-17 and SLAM have opposing effects on IFN-gamma production through CREB activation in persons with tuberculosis.
干扰素-γ(IFN-γ)对于抵抗结核分枝杆菌至关重要,转录因子环磷酸腺苷反应元件结合蛋白(CREB)可增加IFN-γ的转录。我们确定了跨膜受体信号淋巴细胞激活分子(SLAM)和白细胞介素-17(IL-17)是否影响结核病患者的CREB磷酸化和IFN-γ产生。当用结核分枝杆菌激活结核病患者的T细胞时,80%的SLAM(+) T细胞表达磷酸化的CREB,并且SLAM激活增加了CREB磷酸化和IFN-γ产生。相比之下,IL-17下调了SLAM表达、CREB磷酸化和IFN-γ产生。因此,在结核病患者中,IL-17和SLAM通过激活CREB对IFN-γ产生具有相反的作用。