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To clarify the components of cellular immunity responsible for defense against the clonal development of myeloma cells, we tested the capacity of human peripheral blood lymphocytes (PBLs) to inhibit the growth of 3 human myeloma cell lines (RPMI 8226, OPM-1, and OPM-2). RPMI 8226 was found to be sensitive to PBLs, showing almost complete growth arrest when cultured with PBLs for 72 h. Inhibition of the growth of RPMI 8226 cells required direct cell-to-cell contact but not presensitization of the PBLs to the target cells, and did not depend on the generation of soluble factors. CD3+, CD4-, CD8- and CD16- cells were found to be the major subset contributing to inhibition of the growth of RPMI 8226 cells, and this growth inhibition was cytostatic rather than cytotoxic. These characteristics distinguished it from growth inhibition mediated by the natural killer system. Impaired PBL-mediated growth inhibition of RPMI 8226 cells was found in patients with various hematologic diseases, including myeloma. It therefore appears that the CD3+, CD4-, CD8- and CD16- cell subset might be involved in tumor immunity in myeloma.

Autologous mixed lymphocyte reaction (AMLR)-induced suppressor function was studied in 12 patients with chronic idiopathic thrombocytopenic purpura (ITP). The function was found to be significantly impaired (20 +/- 55%; p less than 0.005) compared with normal subjects (69 +/- 25%). AMLRs in these patients were significantly decreased (p less than 0.05) compared with normal subjects. There was no significant correlation between AMLR-induced suppressor function and platelet counts. Nine patients were studied for AMLR-induced suppressor function before and after splenectomy. The platelet counts increased significantly as a result of splenectomy, but the AMLR-induced suppressor function showed no significant improvement. The results of this study suggest that suppressor dysfunction in ITP may be an immunologic defect irrespective of disease activity. We consider that this abnormality may reflect in vivo failure of the immunoregulatory (feedback) mechanism in ITP.

Neoplastic cells of 18 patients with multiple myeloma were studied using a panel of 6 monoclonal antibodies to B cells and monospecific antisera against the light chain types of immunoglobulin. OKT10 bound to the myeloma cells of all the patients, although only a small percentage of the cells reacted in 3 instances. Monoclonal sIg was present in 5 patients. HLA-DR antigen detected with OKIa-1 was found in 5 patients. B1 bound to a small percentage of the myeloma cells only in 2 patients who had received treatment. The B1+ cells were always sIg+. In 3 patients, BA-2 reacted with the myeloma cells. BA-1 and BA-3 invariably did not react with the cells. Myeloma cells with B cell markers were found more frequently in treated patients than in untreated patients. The RPMI8226 line was also studied and found to react with OKT10 and BA-2. The results of this study show the presence of phenotypic variety in myeloma cells.

Ultrastructures of normal T-cell subpopulations, Tγ and Tμ cells, were studied. Tγ cells were isolated and identified by repeating the rosetting method; firstly, by E rosette formation with neuraminidase-treated sheep red blood cells (SRBC), and next by EAy-rosette formation with ox red blood cells coated with IgG antibody (EAox). Before EAox rosetting, SRBC on isolated T cells were lysed by autologous plasma instead of ammonium chloride solution. Normal Tγ cells were heterogeneous with regard to their granules; the majority of Tγ cells had parallel tubular arrays (PTA) and a few had electron-dense granules. When ammonium chloride solution was employed to lyse SRBC, PTA were never observed; PTA in normal Tγ cells and in chronic lympho-cytic leukemia cells with Tγ character both seemed to change into electron-dense granules after ammonium chloride treatment. In contrast to Tγ cells, Tμ cells were characterized by clustered dense bodies, i.e. focal aggregates of electron-dense granules.