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Kenneth P. Johnson, MD; George Belendiuk, MD, PhD

Arch Neurol. 1985;42(11):1043-1044.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Baltimore; East Hanover, NJ

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