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T Kanoh

Publications and source records attributed to T Kanoh.

At least 181 records · Page 10Linked to original sources
PubMed1987

Inhibitory mechanism of the proliferative responses of resting B cells: feedback regulation by a lymphokine (suppressive B-cell factor) produced by Fc receptor-stimulated B cells.

We investigated the effect of a lymphokine termed 'suppressive B-cell factor' (SBF), which is produced by FcR gamma (Fc receptor for IgG)-stimulated B cells or hybridoma TS4.44, and is known to suppress B-cell responses in vivo and in vitro by inhibiting their proliferation. Small B cells, fractionated by Percoll density gradient, from athymic nude mice (BALB/c) secreted SBF after binding EA (sheep erythrocytes sensitized with IgG mouse anti-sheep erythrocyte antibody), and the proliferation of small but not large B cells was preferentially suppressed by SBF in response to LPS in vitro. Proliferation of purified B cells from BALB/c nu/nu mice, induced by a synergistic interaction between F(ab')2 fragment of goat anti-mouse IgM antibody and B-cell stimulating factor (BSF1), was almost completely abrogated by the co-existence of SBF during the 72-hr culture period. However, the co-culture with SBF for the last 24 or 48 hr, as well as of B cells pretreated with SBF for 1 hr at 37 degrees, partially inhibited the growth response. These findings suggest that SBF operates on resting B cells and holds them in a resting state. This notion would be further supported by the fact that SBF inhibited G0-G1 transition. Taken together, we conclude that SBF acts on the early step of B-cell activation, thereby inhibiting B-cell growth. Arrest of resting B cells in the G0 phase and failure of an increase in functional receptors for BSF1 seem to be responsible for the suppression of B-cell responses.

Animals↗
PubMed1987

Selective IgM deficiency in adults: phenotypically and functionally altered profiles of peripheral blood lymphocytes.

Peripheral blood lymphocytes from four patients with selective IgM deficiency were examined phenotypically and functionally. Although B cell subpopulations determined by surface immunoglobulins were within normal or nearly normal range, T8+ cells were significantly increased and T4/T8 ratios were inverted in three patients. IgM specific hyporesponsiveness in the PWM-driven immunoglobulin production system was observed in all four patients. Ia-like antigen positive T cells were increased in two patients; both had increased Leu2a+ Leu15+ suppressor-effector cells. In addition, Leu3a+ Leu8+ suppressor-inducer cells were increased in one of these two patients. Excessive (either IgM-specific or isotype non-specific) suppressor activity of T cells and IgM specific hyporesponsiveness of non-T cells were observed in these two patients in the recombination plaque assay. Although these results showed the complexity of the pathogenesis of this syndrome, they suggested that suppressor-associated T cells may play a role in some patients with selective IgM deficiency.

Adult↗
PubMed1987

Phospholipid base exchange activity in the leukocyte membranes of patients with inflammatory disorders.

Phospholipid base exchange and cholinephosphotransferase (CPT) and ethanolaminephosphotransferase (EPT) activities were assessed in the membranes of neutrophils or lymphocytes from patients with various inflammatory disorders. Ethanolamine exchange activity was significantly enhanced in both neutrophils and lymphocytes from patients with active Behçet's disease, active systemic lupus erythematosus (SLE), and severe bacterial infections and slightly enhanced in those from patients with active rheumatoid arthritis (RA), compared with healthy controls. No abnormal findings were found in CPT, EPT, or serine or choline base exchange activities in the leukocytes from any of the diseased groups tested or in the ethanolamine exchange activity of patients with severe viral infections and inactive SLE, RA, and Behçet's disease. The authors have recently demonstrated the enhancement of transmethylation and phospholipase A2 activity in human leukocyte membranes at the height of inflammatory disease states, as well as the activation of leukocyte ethanolamine exchange by bioactive stimulants. These data postulate that phosphatidylethanolamine synthesis by the base exchange reaction may be the precursor of transmethylation and its subsequent activation of phospholipase A2, leading to the induction of arachidonic acid cascade.

Adolescent↗
PubMed1987

Detection of mutagenic compounds in the urine of mice administered pyrene during exposure to NO2.

The urine of mice injected intraperitoneally with pyrene during exposure to NO2 was found to contain highly mutagenic compounds by means of the Ames test using Salmonella typhimurium strain TA98. The mice were exposed to 20 ppm NO2 for 3 days before intraperitoneal injection of pyrene (800 mg/kg of body weight). The pyrene-treated mice were further exposed to NO2 for an additional 24 hr, and the urine from the mice was collected in ice-cooled containers and stored frozen in the dark. The collected samples were treated with beta-glucuronidase and passed through activated Sep-Pack C18 cartridges. After elution with methanol, the effluent was concentrated and the residue was dissolved in dimethyl sulfoxide (DMSO). The DMSO solution was fractionated by high-performance liquid chromatography and the mutagenicity of each fraction was assayed with S. typhimurium strain TA98. The mutagenic compounds 3-hydroxy-1-nitropyrene, 6-hydroxy-1-nitropyrene, 8-hydroxy-1-nitropyrene, and 1-hydroxypyrene were identified in the mutagenic fractions by mass spectrometry and UV-visible spectrophotometry with synthetic reference substances. These mutagenic compounds may have been formed by either nitration of hydroxylated pyrene, or hydroxylation of 1-nitropyrene, which is formed in vivo from pyrene and NO2, or the simultaneous occurrence of these two reactions in the mouse body.

Animals↗
PubMed1987

Renal plasmacytoma.

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Gallium Radioisotopes↗
PubMed1986

The physicochemical properties and the process of pyrogel formation of IgD pyroglobulin.

The extremely rare IgD pyroglobulin caused opalescence, lost its antigenicity and acquired more negative charge when heated for 30 min at 56 degrees C. Exposure to 60 degrees C for 60 min produced a firm gel. The thermoprecipitability was abolished by the treatment with guanidine, urea and sodium dodecyl sulfate, but not by 2-mercaptoethanol or neuraminidase, and required the presence of both heavy and light chains. However, amino acid analysis showed abnormalities only in the heavy chain. We hypothesize that the irreversible heat-induced aggregation of IgD pyroglobulin is the result of a conformational change, triggered by light chain, which increases the molecular hydrophobicity.

Aged↗