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 tuberculin 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 Hodgkin's disease (12) has further emphasized the extent of the immunological defect. The purpose of the present communication is to inquire how intimately, and with what consistency, loss of the delayed type of hypersensitivity is associated with Hodgkin's disease and to pose certain questions regarding the causal relationships. Dinitrochlorobenzene (13, 14), a compound which uniformly induces hypersensitivity 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 dinitrochlorobenzene permits the evaluation of the state of the delayed sensitivity mechanism in the individual Hodgkin's patient. Several previous investigators (15-17) have studied small groups of patients with Hodgkin's disease and other lymphomas 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 associated with a loss of delayed hypersensitivity,