Becher B, Giacomini P S, Pelletier D, McCrea E, Prat A, Antel J P
Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Quebec, Canada.
Ann Neurol. 1999 Feb;45(2):247-50.
Interferon-gamma (IFN-gamma) is implicated as a participant in the immune effector and regulatory mechanisms considered to mediate the pathogenesis of multiple sclerosis (MS). We have used an intracellular cytokine staining technique to demonstrate that the proportion of ex vivo peripheral blood CD4 and CD8 T-cell subsets expressing IFN-gamma is increased in secondary progressing (SP) MS patients, whereas the values in untreated relapsing-remitting (RR) MS patients are reduced compared with those of controls. Patients treated with interferon-beta (IFN-beta) have an even more significant reduction in the percentage of IFN-gamma-secreting cells. The finding that the number of IFN-gamma-expressing CD8 cells is increased in SPMS patients, a group with reduced functional suppressor activity, and is most significantly reduced by IFN-beta therapy, which increases suppressor activity, indicates that IFN-gamma secretion by CD8 T cells and functional suppressor defects attributed to this cell subset in MS can be dissociated.
γ干扰素（IFN-γ）被认为是参与介导多发性硬化症（MS）发病机制的免疫效应和调节机制的一个因素。我们采用细胞内细胞因子染色技术来证明，在继发进展型（SP）MS患者中，表达IFN-γ的离体外周血CD4和CD8 T细胞亚群的比例增加，而未经治疗的复发缓解型（RR）MS患者的值与对照组相比降低。接受β干扰素（IFN-β）治疗的患者分泌IFN-γ的细胞百分比甚至有更显著的降低。在功能抑制活性降低的SPMS患者中，表达IFN-γ的CD8细胞数量增加，而通过增加抑制活性的IFN-β治疗后该数量降低最为显著，这一发现表明MS中CD8 T细胞分泌IFN-γ与归因于该细胞亚群的功能抑制缺陷可以分离。
