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Infect Immun. 1973 May; 7(5): 764-770
Copyright © 1973 American Society for Microbiology. All Rights Reserved.
a Department of Microbiology, The Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27103
ABSTRACT
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.
1 Present address: Research Unit, Wood VA Hospital, Wood (Milwaukee), Wis. 53193.
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