Abstract
THE delayed hypersensitivity (DH) reaction seems to be enhanced by treatment with cyclophosphamide and this has been discussed in the context of depression of antibody production1–4. Askenase et al.5, however, reported that low doses of cyclophosphamide augmented the reaction to sheep erythrocytes without affecting antibody production. Polak and Turk6 suggested that cyclophosphamide could break down immunological tolerance to the dinitrophenyl group, as measured by a skin reaction in guinea pigs after treatment with the drug to inhibit suppressor cells. The nature of the suppressing cells was not clear at the time. We report here that treatment of mice with cyclophosphamide also significantly affects DH reaction to methylated human serum albumin (MHSA)7 which induces little antibody production, and that the enhanced DH reaction is caused by damage to T rather than B cells. Independent recovery, from the damage due to cyclophosphamide, by individual subpopulations of T cells accounts for the kinetics of this phenomenon.
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