Several informative studies have described the use of immunosuppressive agents in diseases classified as auto-immune in pathogenesis. Dameshek and Schwartz¹,²have shown that certain antimetabolities are capable of creating a drug-induced immunologic tolerance that theoretically should reduce the activity of diseases produced by altered immune mechanisms. Various immunosuppressive agents have been observed experimentally to reduce or prevent the primary³,⁴and secondary⁵immune response in animals, decrease the level of γ-globulin,⁶inhibit immediate and delayed hypersensitivity,⁷and to induce a prolonged functionalsurvival state in homograft material.⁸,⁹Furthermore, various clinical trials¹⁰⁻¹³suggest potential beneficial effects of immunosuppressive agents in diseases such as systemic lupus erythematosus, auto-immune hemolytic anemia, hyperglobulinemia purpura, erythema nodosum, and polyarteritis nodosa, identified with immunologic mechanisms. One of these agents, azathioprine (Imuran)¹⁴,¹⁵has shown sufficient promise to justify a clinical trial in ulcerative colitis. Azathioprine is a heterocyclic derivative of 6-mercaptopurine
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Gerald E. Bowen (1966) studied this question.