[A case of IgD (lambda)-multiple myeloma presenting as a tonsillar tumor, characterized by various kinds of inclusions in the tumor cells as an initial manifestation].
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Biomedical subjects
Publications and source records attributed to T Kanoh.
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The effect of polymorphonuclear leukocytes (PMNs) on lymphocyte subpopulations and their reactivity was investigated by adding supernatants obtained by culturing PMNs with allogeneic or autologous lymphocytes which had been pre-treated with prostaglandin (PG) synthetase inhibitors. PMNs were obtained from 12 healthy individuals, 7 patients with systemic lupus erythematosus (SLE) and 6 patients with bacterial infections. Freshly prepared normal lymphocytes pretreated with PG synthetase inhibitors were incubated with the above supernatants, and the lymphocyte and T-lymphocyte subpopulations were then quantitated, the responses of lymphocytes to mitogens measured and the generation of helper and suppressor T-cell activities for PWM-stimulated cultures assessed. We also ascertained which T-cell population, i.e. OKT4+ or OKT8+ cells, which had been altered by incubation with supernatants, was responsible for the suppressor T-cell activity. A reduced per cent of OKT4+ cells; depressed responses to Con A, PHA, PWM and allogeneic lymphocytes, impaired helper T-cell activity; and increased suppressor T-cell activity were noted after incubation of lymphocytes with supernatants. The percentage of T lymphocytes and of OKT8+ cells was, however, not affected. Further, enhanced suppressor T-cell activity was obtained when supernatant-incubated OKT4+ cells were cultured with OKT8+ cells, regardless of whether the latter had previously been exposed to supernatants. Addition of PG inhibitors to PMN co-cultures nearly restored the original percentage and reactivity of the T-lymphocyte populations, indicating a role for PG released from PMNs in the effects observed. The amount of PG demonstrated in co-culture supernatants was 30 times more than obtained by sonification of fresh PMNs and 10 times more than found in the culture medium containing PMNs alone. These results suggest that, besides monocytes, other phagocytes, including PMNs, can modulate lymphocyte-mediated immune reactivity by the release of PG. Deceased number of OKT4+ cells, impaired helper T-cell activity and enhanced suppressor cell activity may, at least in part, result from the effect of PG released from PMNs as well as monocytes.
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A case of gastric plasmacytoma is reported in an 81-year-old woman. Immunofluorescent and immunoelectrophoretic studies showed that the tumor cells produced IgM-lambda molecules, whereas no monoclonal immunoglobulin could be detected both in the serum and in the urine. Of more than 60 reported cases of gastric plasmacytoma, only a few reports referred to the production of monoclonal immunoglobulin by the tumor cells. This case is the first one of IgM-producing gastric plasmacytoma. Moreover, the produced IgM was found to be 7S-IgM. It is extremely rare that 7S-IgM alone is detected in the absence of 19S-IgM.
Needle-like, rod-shaped, and rhomboid intracytoplasmic crystalline inclusions were found in myeloma cells from the bone marrow of a patient with IgA-kappa and Bence Jones-kappa type multiple myeloma. Cytochemical, immunochemical, and electron microscopic studies revealed that these inclusions consisted of at least three kinds of components: kappa light chain crystals, lysosomal enzymes, and amyloid fibrils. The coexistence of these three kinds of inclusions in one myeloma cell suggests an intracellular site for the formation of amyloid fibrils. From these observations, the authors postulated that the excessively produced light chains were transported to the Golgi apparatus where they were transformed into crystalline inclusions, and thereafter, digested by lysosomal enzymes to form amyloid fibrils. The demonstration of crystalline inclusions which reacted exclusively with antisera against free light chains indicates that the Bence Jones protein is a precursor of amyloid light chain.
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We assessed the generation of reactive oxygen species (ROS: O2-, H2O2, OH . , chemiluminescence) by neutrophils and monocytes from six patients with infectious mononucleosis, ten patients with other viral diseases, and ten normal controls. Neutrophils from infectious mononucleosis patients showed markedly decreased generation of all reactive oxygen species, compared with the two control groups; this abnormality persisted for four to eight weeks after disease onset. Monocytes from these patients generated normal levels of ROS. Normal neutrophils incubated with T lymphocytes from infectious mononucleosis patients generated significantly less of each ROS than did those incubated with T cells from either control group. T cell-mediated suppression of ROS generation required both OKT4+ cells from infectious mononucleosis patients and OKT8+ cells from either patients or normals. We conclude that the generation of reaction oxygen species in neutrophils is suppressed in patients with infectious mononucleosis, at least in part, by interacting subsets of T lymphocytes.
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The synthesis of J chain and the ultrastructural changes in chronic lymphocytic leukaemia (CLL) cells during in vitro cultures stimulated with PWM and/or allogenic T cells were investigated by immunoelectron microscopy, radioimmunoassay and anti-idiotype antibodies, in an attempt to demonstrate changes in the maturation stage of CLL cells. The cells from four patients showed the induction of J chain synthesis in parallel with the increase of Ig synthesis. Two of revealed cytological transformations, in which CLL cells resembled immunoblasts or plasmacytoid cells. These findings suggest that some CLL cells are not 'frozen' within the original maturation stage and can be induced to differentiate to a more mature stage.