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The role of local pulmonary delayed hypersensitivity in accelerated pulmonary granuloma formation was investigated using cortisone acetate, an immunosuppressive drug that appears to preferentially eliminate committed lymphocytes at appropriate doses. Data are presented showing that cortisone acetate suppressed local pulmonary delayed hypersensitivity at the time of and subsequent to challenge with BCG. Furthermore, cortisone damage appeared to involve primarily committed lymphocyte populations since the defect was repairable with sensitized spleen cells, an unlikely source of macrophage precursors.

Relationship of BCG-Induced Pulmonary Delayed Hypersensitivity to Accelerated Granuloma Formation in Rabbit Lungs: Effect of Cortisone Acetate