Human TcRγδ+ lymphocyte response on primary exposure to Plasmodium falciparum

Abstract

SUMMARY In 29 patients experiencing their first P. falciparum malarial attack. blood levels of TcRγδ+ lymphocytes were studied from the onset of infection to up to 6-9 months later. Blood TcRγδ+ lymphocytes, revealed using the TcRδ1 monoclonal antibody (MoAb) were increased both in absolute and relative numbers. Alterations lasted for up to 3-4 months following the attack. A TiγA/ BB3 reactive Vγ/9 subset was preferentially amplified, in vitro, TcRγδ+ lymphocytes from both malaria-sensitized and unprimed donors responded to P. falciparum schizont extract (PFSE). PFSE-stimulated polyclonal T cell lines consisted principally in TcRγδ+ cells with a TiγAd+/BB-3+ phenotype. Several TcRγδ+ 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 Vγ9 subset. In long-term cultures. TcRγδ+ 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 TcRγδ+, PFSE-specific T lymphocyte clones. This suggests that regulatory interactions occur between activated TcRγδ+ and TcRγβ+ cells generated by P. falciparum. Sequential variations in blood TcRγδ+ and TcRγβ+ lymphocyte levels after primary exposure to P. falciparum suggest that such regulatory interactions may occur in vivo.