Studies of IFN, IL-1, and Tnf on Induction of Differentiation and Activation of Neutrophils.

实验主要是研究IFN和TNF对白血病细胞系增殖和分化的影响，以及这些细胞因子对人外周血中性粒细胞活化的影响。实验结果如下：1。IFN和TNE对人白血病细胞系增殖的影响。(1) IFN和TNF抑制人白血病细胞株ML-1、U-937的增殖。(2) IFN和TNF分别诱导人白血病细胞系分化。(3) TNF和tgf - β联合诱导人白血病细胞系的分化可叠加或协同作用。但TNF受体未见变化。(4)在U-937细胞中，TNF和tgf - β均可在1小时内降低myc mRNA的表达。当TNF与tgf - β联合使用时，TNF可增加或协同降低myc mRNA的表达。IFN、IL-1和TNF对外周中性粒细胞功能的影响。研究了细胞因子（ifn - β和γ， il -1 α和β， IL-2， TNF, G-CSF）对PMA或opsonized zymosan刺激人中性粒细胞生成超氧化物（O^-_）的影响，并考察了这些细胞因子的活化活性。(1) ifn - γ、IL-1、TNF和G-CSF均能促进O^-_型人外周血中性粒细胞的生成，其中inf - γ的作用最大。而IFN-rho和IL-2则无明显影响。(2)利用ifn - γ作为细胞因子，研究了增强中性粒细胞功能的机制，提示Ca^<++>内流到胞浆中可能是激活中性粒细胞功能的重要因素。

The experiments have been mainly undertaken to examine the effects of IFN and TNF on proliferation and differentiation of leukemia cell lines, and the effects of these cytokines on the activation of human peripheral neutrophils. Results obtained are as follows :1. The effects of IFN and TNE on proliferation of human leukemia cell lines.(1) Proliferation of human leukemia cell lines (ML-1, U-937) was inhibited by IFN and TNF.(2) IFN and TNF induced differentiation of human leukemia cell lines, respectively.(3) Differentiation of human leukemia cell lines was additively or synergistically induced by combination of TNF and TGF-beta. However, change of TNF receptors was not observed.(4) In U-937 cells, either TNF and TGF-beta alone decreased myc mRNA expression within one hour. When combined with TGF-beta, TNF additively or synergistically decreased myc mRNA expression.2. The effects of IFN, IL-1, and TNF on peripheral neutrophil functions. The effects of cytokines (IFN-betaandgamma, IL-1alphaandbeta, IL-2, TNF, G-CSF) on the generation of superoxide (O^-_) of human neutrophils stimulated by PMA or opsonized zymosan were investigated to examine the activation activities of these cytokines.(1) IFN-gamma, IL-1, TNF and G-CSF enhanced the production of O^-_ form human peripheral neutrophils and INF-gamma was most effective. However, IFN-rho and IL-2 showed no effect.(2) The mechanism of enhancement of neutrophil functions was investigated by using IFN-gamma as a cytokine and it is suggested that influx of Ca^<++> into cytoplasma may be important to activate neutrophil functions.