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Impairment of T‐Helper Function by a Plasmodium berghei ‐Derived Immunosuppressive Factor 1
Author(s) -
SROUR EDWARD F.,
SEGRE MARIANGELA,
SEGRE DIEGO
Publication year - 1988
Publication title -
the journal of protozoology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 0022-3921
DOI - 10.1111/j.1550-7408.1988.tb04127.x
Subject(s) - keyhole limpet hemocyanin , plasmodium berghei , antigen , immunology , in vitro , hemocyanin , biology , antibody , immune system , microbiology and biotechnology , malaria , biochemistry
Mice injected with an immunosuppressive factor (ISF) extracted from Plasmodium berghei ‐infected rat erythrocytes have a reduced antibody response to unrelated antigens. T‐cells from ISF‐treated mice failed to provide adequate help to naive, syngeneic B‐cells in the primary IgM response in vitro to sheep red blood cells and to dinitrophenylated keyhole limpet hemocyanin. The same T‐cells, however, were able to cooperate with memory B‐cells in the secondary IgG response. No other cellular deficit was delected in ISF‐treated mice; B‐cells and macrophages behaved normally, and there was no detectable excess of suppressor cells. The T‐cell impairment was not reflected in decreased production of interleukin 2, but was also shown by the diminished delayed type hyperaensitivity reaction to sheep red blood cells of ISF‐treated mice.