Premium
Cyclosporin A Inhibits Induction but Not Production of Gamma Interferon Induced by Epstein–Barr Virus
Author(s) -
ANDERSSON J. P.,
ANDERSSON U. G.,
BRITTON S. F.,
LEY M. DE
Publication year - 1985
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.1365-3083.1985.tb01872.x
Subject(s) - virus , in vivo , in vitro , polyclonal antibodies , interferon , epstein–barr virus , biology , interferon gamma , virology , immunology , immune system , antigen , biochemistry , microbiology and biotechnology
Cyclosporin A (CsA) interferes with various T‐cell functions in vitro and is a potent inhibitor of T‐cell‐dependent reactions in vivo, such as graft rejection and control of virus infections. Since human gamma interferon (Hu IFN‐γ) is synthesized by T cells and has a controlling role in regulation of Epstein–Barr virus (EBV) infection, we have studied the effects of CsA on EBV‐induced cellular Hu IFN‐γ release. CsA inhibited dose‐dependently the EBV‐induced Hu IFN‐γ response, studied at the cellular level in human blood lymphocytes. These effects were not due to toxicity of CsA, since at inhibitory levels cellular EBV infection measured as polyclonal IgM production proceeded unaffected. CsA did not affect the number of spontaneous Hu IFN‐γ‐secreting cells, nor did it have any inhibitory effect if added after virus exposure. It is concluded that CsA inhibits induction but not production of cellular Hu IFN‐γ.