HUMAN TCR-GAMMA-DELTA(-RESPONSE ON PRIMARY EXPOSURE TO PLASMODIUM-FALCIPARUM() LYMPHOCYTE)

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 l asted for up to 3-4 months following the attack. A Ti gamma A/ BB3 rea ctive V gamma 9 subset was preferentially amplified. In vitro, TcR gam ma delta(+) lymphocytes from both malaria-sensitized and unprimed dono rs responded to P.falciparum schizont extract (PFSE). PFSE-stimulated polyclonal T cell lines consisted principally in TcR gamma delta(+) ce lls with a Ti gamma A(+)/BB3(+) phenotype. Several TcR gamma delta(+) T cell clones obtained from patients recovering from acute malarial at tack 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 PF SE 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 be tween activated TcR gamma delta(+) and TcR alpha beta(+) cells generat ed 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 .