Roussilhon C, Agrapart M, Guglielmi P, Bensussan A, Brasseur P, Ballet J J
Laboratory of Experimental Parasitology, Institute Pasteur, Paris, France.
Clin Exp Immunol. 1994 Jan;95(1):91-7. doi: 10.1111/j.1365-2249.1994.tb06020.x.
In 29 patients experiencing their first P. falciparum malarial attack, blood levels of TcR gamma delta+ lymphocytes were studied from the onset of infection to up to 6-9 months later. Blood TcR gamma delta+ lymphocytes, revealed using the TcR delta 1 monoclonal antibody (MoAb), were increased both in absolute and relative numbers. Alterations lasted for up to 3-4 months following the attack. A Ti gamma A/BB3 reactive V gamma 9 subset was preferentially amplified. In vitro, TcR gamma delta+ lymphocytes from both malaria-sensitized and unprimed donors responded to P. falciparum schizont extract (PFSE). PFSE-stimulated polyclonal T cell lines consisted principally in TcR gamma delta+ cells with a Ti gamma A+/BB3+ phenotype. Several TcR gamma delta+ T cell clones obtained from patients recovering from acute malarial attack were maintained in the presence of PFSE and autologous irradiated PBL. They belong to the V gamma 9 subset. In long-term cultures, TcR gamma delta+ clones progressively lost their capacity to react to PFSE antigen while they were able to proliferate and to exert cytotoxic activity in response to autologous TcR alpha beta+, PFSE-specific T lymphocyte clones. This suggests that regulatory interactions occur between activated TcR gamma delta+ and TcR alpha beta+ cells generated by P. falciparum. Sequential variations in blood TcR gamma delta+ and TcR alpha beta+ lymphocyte levels after primary exposure to P. falciparum suggest that such regulatory interactions may occur in vivo.
在29例首次发生恶性疟原虫疟疾发作的患者中，研究了从感染开始直至6 - 9个月后血中TcRγδ +淋巴细胞水平。使用TcRδ1单克隆抗体（MoAb）检测发现，血中TcRγδ +淋巴细胞的绝对数量和相对数量均增加。这种变化在发作后持续长达3 - 4个月。一个TiγA/BB3反应性Vγ9亚群被优先扩增。在体外，来自疟疾致敏和未致敏供体的TcRγδ +淋巴细胞对恶性疟原虫裂殖体提取物（PFSE）均有反应。PFSE刺激的多克隆T细胞系主要由具有TiγA + /BB3 +表型的TcRγδ +细胞组成。从急性疟疾发作康复的患者中获得的几个TcRγδ + T细胞克隆在PFSE和自体照射的外周血淋巴细胞（PBL）存在的情况下得以维持。它们属于Vγ9亚群。在长期培养中，TcRγδ +克隆逐渐失去对PFSE抗原反应的能力，而它们能够对自体TcRαβ +、PFSE特异性T淋巴细胞克隆的刺激进行增殖并发挥细胞毒性活性。这表明在恶性疟原虫产生的活化TcRγδ +和TcRαβ +细胞之间发生了调节性相互作用。初次接触恶性疟原虫后血中TcRγδ +和TcRαβ +淋巴细胞水平的序列变化表明这种调节性相互作用可能在体内发生。
