Limb G A, Brown K A, Wolstencroft R A, Ellis B A, Dumonde D C
Department of Immunology, Rayne Institute, United Medical and Dental Schools, St. Thomas' Hospital, London.
Clin Exp Immunol. 1988 Nov;74(2):171-6.
The decrease in Fc-receptor-positive cells that occurred during a 6 h incubation of resident and elicited guinea-pig macrophages was partly abrogated when lymphokines were present in the culture. When the same lymphokine preparations were tested on C3b receptor-expression they preferentially sustained the percentage of C3b rosettes formed by resident rather than elicited macrophages. This lymphokine-induced maintenance of Fc and C3b rosettes by cultured macrophages may have been due to an inhibition of receptor release or an increase in receptor synthesis. Supernatants from cultured macrophages contain shed Fc and C3b receptors which inhibit rosette formation by other macrophages. From the demonstration that culture supernatants from both lymphokine-treated and untreated macrophages significantly inhibited Fc and C3b rosette formation by freshly obtained macrophages it seems that the shedding of Fc and C3b receptors is not modified by lymphokines. The maintenance of Fc and C3b rosettes by lymphokines was inhibited by treatment of the macrophages with cycloheximide, suggesting that the lymphokine effect was due to an increase in synthesis de novo of the Fc and C3b receptors. The lymphokine-inducing antigens, BGG and PPD, and control lymphokine preparations were devoid of receptor modifying activity. The reduction in the percentage of Fc rosettes after 6 h culture appears to be due to a loss of Fc receptors for IgG1. Although lymphokines partly inhibited this effect they could not prevent the loss of these receptors following 24 h culture, unlike their action in augmenting the expression of Fc receptors for IgG2. These findings suggest that a selective enhancement of Fc receptor synthesis by lymphokines may modify the functional activities of macrophages.
在驻留和诱导的豚鼠巨噬细胞6小时培养过程中出现的Fc受体阳性细胞减少现象,当培养物中存在淋巴因子时,部分得到了消除。当对相同的淋巴因子制剂进行C3b受体表达测试时,它们优先维持驻留巨噬细胞而非诱导巨噬细胞形成C3b玫瑰花结的百分比。培养的巨噬细胞由淋巴因子诱导的Fc和C3b玫瑰花结维持现象,可能是由于受体释放受到抑制或受体合成增加。培养的巨噬细胞上清液含有脱落的Fc和C3b受体,它们会抑制其他巨噬细胞形成玫瑰花结。从淋巴因子处理和未处理的巨噬细胞培养上清液均能显著抑制新鲜获得的巨噬细胞形成Fc和C3b玫瑰花结这一现象来看,Fc和C3b受体的脱落似乎不受淋巴因子的影响。用环己酰亚胺处理巨噬细胞可抑制淋巴因子对Fc和C3b玫瑰花结的维持作用,这表明淋巴因子的作用是由于Fc和C3b受体从头合成增加所致。诱导淋巴因子产生的抗原、BGG和PPD以及对照淋巴因子制剂均无受体修饰活性。培养6小时后Fc玫瑰花结百分比的降低似乎是由于IgG1的Fc受体丢失所致。尽管淋巴因子部分抑制了这种作用,但与它们增强IgG2的Fc受体表达的作用不同,它们无法阻止24小时培养后这些受体丢失。这些发现表明,淋巴因子对Fc受体合成的选择性增强可能会改变巨噬细胞的功能活性。