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THE potential for immunosuppressive agents to control the poorly understood pathophysiologic consequences of autoimmunity has intrigued clinical immunologists for decades. Unfortunately, the toxicity of these agents has often outweighed their clinical benefit. In the mid-1970s cyclosporine was shown to have pronounced immunosuppressive activity without causing myelotoxicity or other severe side effects, and it was quickly proved to be effective in a wide variety of animal models of transplantation and autoimmunity.1 During the ensuing years, great strides have been made in understanding the basic immunopharmacology of cyclosporine and in demonstrating its effectiveness in human transplantation and autoimmune disorders.2 In studies using . . .
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Fathman et al. (1992) studied this question.
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