Chizzolini C, Grau G E, Geinoz A, Schrijvers D
Centre International de Recherches Médicales, Fraceville, Gabon.
Clin Exp Immunol. 1990 Jan;79(1):95-9. doi: 10.1111/j.1365-2249.1990.tb05133.x.
Interferon (IFN) alpha and gamma were measured by radio-immunoassays in supernatants from cultures of peripheral blood mononuclear cells (PBMC) or purified T cell subsets incubated with either Plasmodium falciparum schizont-enriched malaria antigen (mAg), uninfected red blood cells (RBC) or pokeweed mitogen (PWM). Cell donors were 24 clinically immune, healthy African adult native residents of a P. falciparum-endemic region, Haut-Ogooué, Gabon, and seven non-immune, European temporary residents with a history of a single to a few malaria infections during the previous 1 to 9 months. When PBMC were cultured in medium alone or with RBC antigen no or low titres of IFN-gamma were detected. PBMC proliferation and IFN-gamma production observed in the presence of mAg were dose dependent and significantly correlated. When cultured with mAg, PBMC from non-immune Europeans produced significantly higher levels of IFN-gamma than did PBMC from clinically immune Africans. No such difference was found when PBMC were cultured with PWM. The mAg-induced IFN-gamma production was due mainly to CD4+ T cells and was not enhanced by CD8+ T cell depletion. No IFN-alpha was detected in culture supernatants. Thus, P. falciparum antigens are able to induce in vitro production of IFN-gamma by CD4+ T cells; however, in this sample, individuals considered to be clinically resistant to malaria were low producers of IFN-gamma.
采用放射免疫分析法检测外周血单个核细胞(PBMC)或纯化的T细胞亚群培养上清液中的干扰素(IFN)α和γ,这些细胞分别与富含恶性疟原虫裂殖体的疟疾抗原(mAg)、未感染的红细胞(RBC)或商陆有丝分裂原(PWM)一起孵育。细胞供体包括24名临床上具有免疫力的健康非洲成年原住民,他们来自加蓬上奥果韦省恶性疟原虫流行地区,以及7名非免疫的欧洲临时居民,这些欧洲人在过去1至9个月内有过1至几次疟疾感染史。当PBMC单独在培养基中培养或与RBC抗原一起培养时,未检测到或仅检测到低滴度的IFN-γ。在mAg存在下观察到的PBMC增殖和IFN-γ产生呈剂量依赖性,且显著相关。当与mAg一起培养时,来自非免疫欧洲人的PBMC产生的IFN-γ水平明显高于来自临床上具有免疫力的非洲人的PBMC。当PBMC与PWM一起培养时,未发现这种差异。mAg诱导的IFN-γ产生主要归因于CD4+T细胞,且不受CD8+T细胞耗竭的增强。在培养上清液中未检测到IFN-α。因此,恶性疟原虫抗原能够在体外诱导CD4+T细胞产生IFN-γ;然而,在这个样本中,被认为对疟疾具有临床抵抗力的个体IFN-γ产生水平较低。