Kaye P M, Sims M, Feldmann M
Clin Exp Immunol. 1986 Apr;64(1):28-34.
In our preceding study, we showed that infection of mice with Mycobacterium microti leads to a dramatic increase in Ia expression on local inflammatory macrophage populations. However, the majority of these cells did not contain intracellular organisms. To evaluate the effect of parasitism of macrophages by M. microti, Ia-induction experiments were performed in vitro. We show here that Ia expression is increased on peritoneal macrophages treated with either crude lymphokine preparations or recombinant gamma-interferon (gamma-IFN) and that this expression is suppressed by M. microti in a dose dependent fashion. The degree of suppression varied between macrophage populations and could be achieved to a lesser extent with killed organisms. It was partially reversed with indomethacin but only poorly so at high infection levels. Inhibition of Ia expression may be of importance in the generation and maintenance of chronic infection.
在我们之前的研究中，我们发现用微小分枝杆菌感染小鼠会导致局部炎性巨噬细胞群体上Ia表达急剧增加。然而，这些细胞中的大多数并不含有胞内生物体。为了评估微小分枝杆菌对巨噬细胞的寄生作用，我们进行了体外Ia诱导实验。我们在此表明，用粗制淋巴因子制剂或重组γ干扰素（γ-IFN）处理的腹膜巨噬细胞上Ia表达会增加，并且这种表达会被微小分枝杆菌以剂量依赖方式抑制。抑制程度在巨噬细胞群体之间有所不同，用灭活生物体也能在较小程度上实现这种抑制。吲哚美辛可部分逆转这种抑制，但在高感染水平时效果不佳。Ia表达的抑制可能在慢性感染的产生和维持中具有重要意义。
