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The human Ia-like antigens, selectively expressed on B lymphocytes, are now recognized to be closely associated with, or identical to, the gene products of the major histocompatibility complex responsible for stimulation in the mixed lymphocyte reaction. The leukemic B lymphocytes of patients with chronic lymphocytic leukemia express these antigens very well. In the present study they were readily detected by several techniques utilizing both allo- and heteroantisera. However, the leukemic B cells from most patients were found to be extremely poor stimulating cells in the mixed lymphocyte reaction. This was particularly apparent when comparisons were made on a B-cell basis with isolated normal B lymphocytes. Leukemic cell death, abnormal kinetics of leukemic cell-mediated stimulation, and serum or cellular suppressor factors do not appear to explain these findings. Studies comparing cells from a leukemic patient with those of her HLA identical sibling and results of mixed lymphocyte reactions between normal and leukemic subjects discordant for D-region-associated Ia antigens ruled out genetic explanations for the differences observed. Experiments with normal peripheral blood mononuclear cells depleted of T cells and monocytes exclude the quantitative deficiency of monocytes which is found in the peripheral blood of most leukemic patients as an explanation. The present results with chronic lymphocytic leukemia cells indicate that the mere expression of the Ia-like antigens by cell populations does not render them effective stimulators. The accumulated evidence obtained indicate that abnormalities, particularly of membrane function and metabolism, known to occur in chronic lymphocytic leukemia lymphocytes may be involved in the poor stimulatory capacity of the leukemic B cells.

Single-stranded DNA (SDNA) occurs in high incidence and in greatest concentration in the sera of patients with systemic lupus erythematosus (SLE), where levels as high as 250 mug/ml were observed. SDNA appears to be an imunogen for anti-SDNA antibodies and forms complexes in vivo of both anti-SDNA-SDNA and anti-NDNA-SDNA types, which apparently play a role in the pathogenesis of the glomerulonephritis found in patients with SLE, SDNA is also found in high incidence but at lower levels in the sera of patients with rheumatoid arthritis. Lesser amounts of SDNA are found in several other diseases in which a low incidence of anti-SDNA antibodies is observed.

Studies on the sera and isolated proteins from 14 patients with gammaG3 multiple myeloma revealed a concentration- and temperature-dependent aggregation which was not encountered in 26 sera from patients with multiple myeloma involving other gammaG subgroups. When the gammaG3 myeloma sera were diluted and characterized by analytical ultracentrifugation, complex formation was minimal. However, when these sera were examined undiluted, marked complex formation was observed. Studies on the isolated proteins, their enzymatic fragments, as well as their heavy and light polypeptide chains localized the aggregating sites to the Fd fragment of the heavy chains. The findings were also documented by acrylamide-gel electrophoresis and capillary tube viscometry.THE HYPERVISCOSITY SYNDROME WAS OBSERVED IN SIX PATIENTS: three with gammaG3 myeloma and three with gammaG1 myeloma. In the latter group extreme protein concentrations appeared essential for the development of the clinical symptoms. The gammaG3 cases, however, because of the aggregation phenomenon, showed the syndrome at relatively low protein concentrations.