Kabilan L, Troye-Blomberg M, Patarroyo M E, Björkman A, Perlmann P
Department of Immunology, University of Stockholm, Sweden.
Clin Exp Immunol. 1987 May;68(2):288-97.
T cells from patients with acute Plasmodium falciparum malaria were investigated for induction of immunoglobulin- or anti-malaria antibody secretion in vitro. Stimulation of autologous T/B cell mixtures (2T:1B) with low concentrations of P. falciparum antigen and cultured for 12 days gave rise to a T-dependent IgG secretion which was significantly elevated over that in medium controls. This was achieved with both a crude P. falciparum antigen and a partially purified preparation enriched in Pf 155, a merozoite-derived antigen deposited in the red cell membrane at invasion (Perlmann et al., 1984). Control antigen (RBC ghosts) induced IgG secretion only when added at high concentrations (greater than 10 micrograms/ml). Neither of the antigens induced IgG secretion at concentrations of less than or equal to 10 micrograms/ml in control cultures of lymphocytes from patients with P. vivax malaria. Supernatants from cultures of P. falciparum patients frequently contained anti-P. falciparum antibodies when nanogram quantities (10-100 ng/ml) of either one of the two malaria antigen preparations was used for stimulation. No anti-P. falciparum antibodies were induced by the control antigen at any concentration. The induced anti-P. falciparum antibodies were directed to intracellular parasites and. at lower frequencies, to Pf 155 as detected on the surface of infected erythrocytes. The induction in vitro of anti-P. falciparum antibodies appeared to be correlated with the presence of such antibodies in the sera of the lymphocyte donors. The lymphocytes of only one out of eight P. vivax patients responded to antigen stimulation by secreting anti-P. falciparum antibodies. However, this donor (but not any of the others), was also P. falciparum seropositive. Taken together, these results indicate that the induction of anti-P. falciparum antibody secretion reflects a secondary response in vitro of cells primed in vivo. The present experimental system should be well suited to map parasite antigen for their capacity to induce T cell dependent responses in P. falciparum malaria.
对急性恶性疟原虫疟疾患者的T细胞进行了体外诱导免疫球蛋白或抗疟疾抗体分泌的研究。用低浓度的恶性疟原虫抗原刺激自体T/B细胞混合物(2T:1B)并培养12天,可产生T细胞依赖性IgG分泌,其水平显著高于培养基对照。使用粗制的恶性疟原虫抗原和富含Pf 155的部分纯化制剂均可实现这一点,Pf 155是一种裂殖子衍生抗原,在入侵时沉积于红细胞膜中(佩尔曼等人,1984年)。对照抗原(红细胞空壳)仅在高浓度(大于10微克/毫升)添加时才诱导IgG分泌。在间日疟患者淋巴细胞的对照培养物中,两种抗原在浓度小于或等于10微克/毫升时均未诱导IgG分泌。当使用两种疟疾抗原制剂之一的纳克量(10 - 100纳克/毫升)进行刺激时,恶性疟患者培养物的上清液中经常含有抗恶性疟原虫抗体。对照抗原在任何浓度下均未诱导产生抗恶性疟原虫抗体。诱导产生的抗恶性疟原虫抗体针对细胞内寄生虫,并且在较低频率下针对感染红细胞表面检测到的Pf 155。体外诱导抗恶性疟原虫抗体似乎与淋巴细胞供体血清中此类抗体的存在相关。八名间日疟患者中只有一名的淋巴细胞通过分泌抗恶性疟原虫抗体对抗原刺激产生反应。然而,该供体(但其他供体均未)也是恶性疟原虫血清阳性。综上所述,这些结果表明抗恶性疟原虫抗体分泌的诱导反映了体内致敏细胞在体外的二次反应。本实验系统应非常适合绘制寄生虫抗原图谱,以了解它们在恶性疟原虫疟疾中诱导T细胞依赖性反应的能力。