Open AccessHuman TcRγδ + lymphocyte response on primary exposure to Plasmodium falciparum
Author(s) -
ROUSSILHON C.,
AGRAPART M.,
GUGLIELMI P.,
BENSUSSAN A.,
BRASSEUR P.,
BALLET J. J.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06020.x
Subject(s) - t cell receptor , immunology , biology , plasmodium falciparum , t lymphocyte , polyclonal antibodies , antigen , cytotoxic t cell , monoclonal antibody , t cell , lymphocyte , virology , antibody , immune system , in vitro , malaria , genetics
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 (PhSE). 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.