Considerable progress in our understanding of the basic mechanisms of delayedtype hypersensitivity has been made in recent years, largely as a consequence of studies in vitro (1, 2). Although most of these studies have approached the problem primarily at the phenomenological level, they have established that the immunological information necessary for the initiation of cell-mediated immune reactions in vitro is possessed by the small lymphocyte which, upon interaction with specific antigens can influence, directly or indirectly, a variety of other cells in its environment.In order to study the cell-mediated immune response on a quantitative basis, we have recently developed a plaque assay which permits determination of the number of antigen-sensitive cells within a population of lymphoid cells (3). The method was designed to detect intrinsic changes produced in sensitized lymphocytes as a consequence of activation by antigen, rather than to measure products secreted by such cells. The basis for our approach is that unstirnulated lymphocytes generally do not support replication of viruses, whereas antigen-activated lymphocytes do so.The quantitative approach to delayed-hypersensitivity reactions in man is of interest at two levels. Because of their importance in the rejection of allografts and tumors, and in the course of some "autoimmune" diseases, there is an urgent need for quantitative measurements in vitro of cell-mediated immunity at the clinical level. We can hardly imagine a clinically useful analysis of an immune response mediated by antibodies if it could be demonstrated only by means of the wheal-and-flare reaction. Yet skin tests are still the principal measure of delayed hypersensitivity in man. Secondly, a method that permits enumeration of specifically sensitized cells is of obvious value for approaching an understanding of the basic mechanisms underlying the delayed-* Recipient of U. S.

In our patient, multiple bilateral nodular pulmonary densities appeared on a chest x-ray at the time of diagnosis of stage IV diffuse lymphocytic lymphoma. After localized radiation therapy, the patient received no further systemic therapy. The pulmonary nodules slowly became larger and more numerous. Nine years later the patient developed proven multiple myeloma. Pulmonary hyalinizing granulomas have not heretofore been associated with proven lymphoreticular neoplasia, although this has long been suspected. The occurrence of two B-cell tumors at different points in time associated with systemic amyloidosis is an extremely rare event. The authors discuss the possibility that these conditions represent an abnormality in a common cell of origin with differing expression over time. Coincidence, however, remains a likely explanation for the different immunopathies that occurred in our patient.

Following conventional surgical management, 100 patients with high risk Stage I melanoma were treated with transfer factor to reduce the incidence of disease recurrence. All patients had primary lesions invasive to Clark's level III or deeper and exceeding 1.0 mm in measured thickness. Ninety-six patients are available for analysis at 15 to 67 months (median: 30 months) after diagnosis. Nine patients have had a recurrence of disease (treatment failure), and one has died. Actuarial non-failure rate is 90%, and survival rate is 99% at five years. A nonrandomized but contemporary control group of 46 patients displaying comparable risk factors was treated with surgery alone. The non-failure rate of this group is 63%, and the survival rate is 69%, data consistent with the results of several published studies. These results suggest that transfer factor immunotherapy may be a valuable adjunct in the treatment of patients with high risk Stage I melanoma.