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In Vitro Effects of Cyclosporin A on Human B‐Cell Responses
Author(s) -
BERGER R.,
MEINGASSNER J. G.,
KNAPP W.
Publication year - 1983
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1983.tb00787.x
Subject(s) - b cell , t cell , biology , cell , pokeweed mitogen , naive b cell , microbiology and biotechnology , cell growth , in vitro , immunology , antibody , antigen presenting cell , immune system , biochemistry , concanavalin a
The in vitro effects of cyclosporin A (CsA) on T‐cell‐dependent and T‐cell‐independent mitogen responses of human B cells were studied. T‐cell‐dependent, pokeweed mitogen (PWM)‐induced B‐cell proliferation and B‐cell differentiation to Ig‐secreting cells were significantly inhibited by CsA, when purified B cells were cultured with T‐cell helper factor containing supernatants instead of T cells. This indicates that the inhibitory effect of CsA on T‐cell‐dependent, PWM‐induced B‐cell proliferation and differentiation is not exclusively due to direct effects on helper T cells. B‐cell proliferations induced by anti‐IgM antibodies and by Staphylococcus aureus bacteria were also found to be sensitive to CsA. Since both types of reactions are T‐cell‐independent, the concept that responses of human B cells can also be affected by CsA in ways that seem to be independent of the well‐documented direct effects of CsA on T cells is further supported. This seems not to be a general phenomenon, however. Epstein‐Barr‐virus‐induced activation of human B cells, as reported previously and also observed by us, is completely insensitive to CsA. It seems, therefore, that certain B‐cell activation mechanisms are sensitive to CsA while others remain unaltered. The difference between these two reaction patterns cannot be exclusively explained by a T‐cell dependence or T‐cell independence of these responses. CsA effects on certain functional B‐cell subsets or interference with accessory cell mechanisms might be responsible.