Studies on delayed hypersensitivity in Hodgkin's disease

The susceptibility of patients with Hodgkin's disease to mycotic and viral infections has long directed attention to an immunological defect in that condition (1). The early finding of tubercu-lin negativity in these patients (2, 3), even in the presence of active tuberculous infection, has been confirmed repeatedly. Subsequent investigations have indicated that this cutaneous anergy extends to many other allergens mediated by the delayed or cellular type of hypersensitivity mechanism (4-11). Recently, the demonstration of tolerance to skin homografts in some patients with Hodg-kin's disease (12) has further emphasized the ex-tent of the immunological defect. The purpose of the present communication is to inquire how intimately, and with what con-sistency, loss of the delayed type of hypersensi-tivity is associated with Hodgkin's disease and to pose certain questions regarding the causal re-lationships. Dinitrochlorobenzene (13, 14), a compound which uniformly induces hypersensi-tivity in normal individuals, has been used in the present investigation to study cutaneous anergy in 37 patients with Hodgkin's disease. Unlike the earlier methods of study, the use of dinitro-chlorobenzene permits the evaluation of the state of the delayed sensitivity mechanism in the indi-vidual Hodgkin's patient. Several previous in-vestigators (15-17) have studied small groups of patients with Hodgkin's disease and other lympho-mas by this method; the present study is the first extensive study of this disease with a technique of active sensitization and the first in which the results have been correlated with the activity of the disease. In the present experiments, active Hodgkin's disease was always found to be asso-ciated with a loss of delayed hypersensitivity