Open AccessPotentiation of in vitro synthesis of human IgE by cyclosporin A (CsA)
Author(s) -
WHEELER D. J.,
ROBINS A.,
PRITCHARD D. I.,
BUNDICK R. V.,
SHAKIB F.
Publication year - 1995
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.1365-2249.1995.tb06640.x
Subject(s) - long term potentiation , peripheral blood mononuclear cell , immunoglobulin e , immunology , in vitro , t cell , pharmacology , medicine , biology , antibody , immune system , biochemistry , receptor
SUMMARY In this study, we investigated the modulatory effects of CsA on in vitro synthesis of IgE. IgG1 and lgG4 by human peripheral blood mononuclear cells (PBMC). In contrast to its known immunosuppressive effect, we have demonstrated that a low dose of CsA (10 −7 M, 120ng/ml) potentiated IgE production by up to 40‐fold (i.e. from 33 ± 4·5 to 1346 ± 290 ng/ml). This potentiation was specific for IgE, since no such effect was demonstrable with IgG1 and IgG4. Potentiation of IgE synthesis by CsA in the PBMC cultures was partly due to CsA acting on T cells, as demonstrated by the addition of CsA‐treated T cells to T cell‐depleted cultures. However, potentiation was also demonstrable in a T cell‐depleted. anti‐CD40‐stimulated culture (four‐fold increase from 400 ± 48 to 1606 ± 127 ng/ml). Our data therefore suggest that there are at least two mechanisms for CsA‐induced potentiation of IgE synthesis, one T cell‐dependent and the other T cell‐independent. The clinical implications of these findings are discussed with regard to the use of CsA in the treatment of Th2‐mcdiated diseases.