Cyclosporine is a biologically active metabolite that is isolated from cultures of the fungal species Tolypocladium inflatam.1 The drug is a potent immunosuppressive agent, which in clinical studies has yielded good results in renal, hepatic, and cardiac transplantation.2-3 Cyclosporine appears to be able to inhibit predominantly T-lymphocyte-dependent immune responses and is capable of inducing transplantation tolerances across major histocompatibility barriers.4-5 Although the exact mode of action of cyclosporine remains unclear, studies indicate that this agent has a differential effect among T-lymphocyte subpopulations. A possible mechanism of action of cyclosporine seems to involve an inhibition of amplification of T-cell immune mechanisms. Recent evidence indicates that this may involve blocking the production or the effect of IL-2 (T-cell growth factor). Both T-cell amplification of cellular immune mechanisms and the generation of T-cell effector cells are, in most cases, dependent on IL-2. Therefore, the inhibition of IL-2 amplification causes
Johnson KP, Belendiuk G. Use of Cyclosporine in Neurological Autoimmune Disease? Arch Neurol. 1985;42(11):1043–1044. doi:10.1001/archneur.1985.04060100025013
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