Karbassi A, Becker J M, Foster J S, Moore R N
J Immunol. 1987 Jul 15;139(2):417-21.
The effect of macrophage colony-stimulating factor (CSF-1) on killing of Candida albicans by murine peritoneal macrophages was determined. The killing capacity of resident peritoneal macrophages was unaffected by CSF-1. However, proteose-peptone-elicited peritoneal exudate macrophages that had been pretreated with CSF-1 (greater than or equal to 1000 U/ml) for 24 or 48 hr exhibited a significantly enhanced capacity to kill C. albicans. CSF-enhanced killing appeared to be independent of endogenously produced interferon-alpha/beta (IFN) in that enhancement by these two agents differed with regard to onset of the effect, target cell responsiveness, and duration of augmented killing. In addition, a highly specific anti-IFN antiserum that totally neutralized IFN augmentation of candidacidal activity had no effect on CSF-induced enhancement. Evidence was obtained indicating that CSF, unlike IFN, augmented mannose-inhibitable binding and ingestion of C. albicans, suggesting that augmented expression of mannose-receptors by CSF-treated macrophages was at least partially responsible for the enhanced killing.
测定了巨噬细胞集落刺激因子(CSF-1)对小鼠腹腔巨噬细胞杀伤白色念珠菌的影响。常驻腹腔巨噬细胞的杀伤能力不受CSF-1的影响。然而,用CSF-1(≥1000 U/ml)预处理24或48小时的蛋白胨诱导的腹腔渗出巨噬细胞对白色念珠菌的杀伤能力显著增强。CSF增强的杀伤作用似乎与内源性产生的α/β干扰素(IFN)无关,因为这两种因子在作用起始、靶细胞反应性和增强杀伤的持续时间方面存在差异。此外,一种能完全中和IFN对杀念珠菌活性增强作用的高度特异性抗IFN抗血清对CSF诱导的增强作用没有影响。有证据表明,与IFN不同,CSF增强了对白色念珠菌的甘露糖抑制性结合和摄取,这表明CSF处理的巨噬细胞中甘露糖受体表达的增加至少部分地导致了杀伤作用的增强。