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Biomedical subjects

K Tanimoto

Publications and source records attributed to K Tanimoto.

At least 343 records · Page 19Linked to original sources
PubMed1977

Reduced Fc-receptor bearing cells in peripheral bloods of patients with systemic lupus erythematosus and in rheumatoid synovial fluids.

Previous reports described that human red cells sensitized with one of Rh antisera (Ripley) make rosette formations (Fc-rosette with some lymphocytes. These Fc-rosettes were well inhibited by aggregated human IgG as well as hypocomplementemic systemic lupus erythematosus (SLE) sera and rheumatoid synovial fluids. In the present study, Fc-receptor bearing lymphocytes were considerably reduced in peripheral bloods of SLE (16.0 +/- 7.6%) and rheumatoid synovial fluids (15.6 +/- 5.3%). On the other hand, EAC-rosette formation rates of peripheral bloods of SLE (32.0 +/- 13.2%) and rheumatoid synovial fluids (30.3 +/- 11.2%) did not significantly differ from normal peripheral bloods (28.3 +/- 2.9%). E-rosette forming lymphocytes were reduced in peripheral bloods of SLE (48.7 +/- 15.7%) and in rheumatoid synovial fluids (49.0 +/- 14.6%) whereas 61.7 +/- 8.6% in normal peripheral bloods. Reduced Fc-rosette formation rates correlated well with the Fc-rosette inhibitory rates. In addition, eluates from the lymphocytes in rheumatoid synovial fluids also inhibited Fc-rosette formation. These results suggested that immune complexes present in peripheral bloods of SLE and rheumatoid synovial fluids are bound to the Fc-receptors on the lymphocytes, block the additional binding of the sensitized red cells, and result in the reduction of Fc-rosette formation.

Antigen-Antibody Complex↗
PubMed1976

Detection of IgG rheumatoid factor by concanavalin A treatment and complement fixation with IgG rheumatoid factor.

Concanavalin A (Con A) froms precipitates with carbohydrate-rich protein such as IgM, IgD, IgE, and IgA. Since IgG contains little carbohydrate and does not react with Con A, the activity of IgG-rheumatoid factor (RF) can be measured in the supernate of the Con A-treated serum. When the latex fixation test (LFT) and the sensitized sheep cell agglutination test (SSCA) were perfromed in the supernate for the detection of IgG-RF, LFT was positive in 32-1% of sera, out of 137 sera originally positive for LFT, and SSCA was positive in 18-5% of sera, out of 119 sera originally positive for SSCA. IgG-RF exhibited lower complement fixing ability than IgM-RF and correlated with agglutination titres of IgG-RF, while the CH50 of the original serum did not correlate with haemolytic activities of either IgM-RF or IgG-RF.

Arthritis, Rheumatoid↗
PubMed1976

Rheumatoid factor-producing cells detected by direct hemolytic plaque assay.

Lymphocytes secreting anti-IgC antibodies, rheumatoid factors (RF), can be detected in the peripheral bloods, synovial fluids, and bone marrows of patients with seropositive rheumatoid arthritis by using a direct plaque-forming cell (PFC) assay with sheep erythrocytes sensitized with reduced and alkylated rabbit IgG hemolysin. The autospecific nature of the RF produced by RF-PFC was indicated by inhibition studies in which the order of patency was human IgG greater than rabbit IgG greater than bovine IgG. In metabolic studies puromycin, cycloheximide, and venblastine suppressed RF-PFC. Cyclic AMP and cyclic GMP were without effect. A need was recognized for using full tissue culture media during the cell separation and plaquing procedures to optimize detection of the RF-PFC. RF-PFC may appear in the blood of patients intermittently despite their continuing presence in the bone marrow. They have been found in the peripheral blood, especially during acutely exacerbating polyarticular synovitis, generalized vasculities, or generally active, aggressive disease. RF-PFC were found in synovial effusions of new or recrduescent acute synovitis. RF-PFC were observed to disappear from the peripheral circulation and the bone marrow during therapy with cytotoxic drugs. The data are consistent with the hypothesis that the appearance of RF-PFC in the peripheral blood represents an anamnestic response to transiently appearing antigen. The nature of the antigen is not specified. The bone marrow may be a site of origin of RF-PFC.

Antibody Specificity↗
PubMed1975

Fc-rosette inhibition by hypocomplementaemic systemic lupus erythematosus sera.

Human red cells sensitized with one of the Rh antisera (Ripley) form rosettes (Fc-rosette) with human B lymphocytes and the rosettes are well inhibited by aggregated human IgG. Since sera of hypocomplementaemic patients with systemic lupus erythematosus (SLE) have frequently been reported to contain immune complexes, they were used for the inhibition of Fc-rosette formation in this study. The results of Fc-rosette inhibition rates of the sera were inversely correlated with the serum CH50 levels. When the sera were separated into top, middle, and bottom fractions by ultracentrifugation, the bottom fractions showed more effective inhititions than the others. Similarly, the strongest inhibition was found in the void volume of the serum separated by Sephadex G200 gel filtration. Reduction and alkylation of IgG resulted in the loss of reactivity with Fc receptor of B lymphocytes, and the rosette inhibiting activities of the SLE sera were markedly reduced after reduction and alkylation. Some of anti-HLA sera were inhibitory for the Fc-rosette formation, while the tested sera did not contain anti-HLA activity assessed by the microcytotoxicity test. These results indicated that circulating immune complexes contained in the sera inhibit the rosette formation, and that the Fc-rosette inhibition test is a simple and relatively sensitive method for the detection of circulating immune complexes. Antinuclear antibody activities of the sera were tested by the indirect immunofluorescent method; however, clear correlations were not obtained between Fc-rosette inhibition rates and staining patterns of antinuclear antibodies. On the other hand, the positive groups of LE-test exhibited slightly greater inhibition rates of the rosette than the negative groups.

Antibodies, Antinuclear↗
PubMed1975

Complement fixation by rheumatoid factor.

The capacity for fixation and activation of hemolytic complement by polyclonal IgM rheumatoid factors (RF) isolated from sera of patients with rheumatoid arthritis and monoclonal IgM-RF isolated from the cryoprecipitates of patients with IgM-IgG mixed cryoglobulinemia was examined. RF mixed with aggregated, reduced, and alkylated human IgG (Agg-R/A-IgG) in the fluid phase failed to significantly reduce the level of total hemolytic complement, CH50, or of individual complement components, C1, C2, C3, and C5. However, sheep erythrocytes (SRC) coated with Agg-R/A-IgG or with reduced and alkylated rabbit IgG anti-SRC antibody were hemolyzed by complement in the presence of polyclonal IgM-RF. Human and guinea pig complement worked equally well. The degree of hemolysis was in direct proportion to the hemagglutination titer of the RF against the same coated cells. Monoclonal IgM-RF, normal human IgM, and purified Waldenström macroglobulins without antiglobulin activity were all inert. Hemolysis of coated SRC by RF and complement was inhibited by prior treatment of the complement source with chelating agents, hydrazine, cobra venom factor, specific antisera to C1q, CR, C5, C6, or C8, or by heating at 56 degrees C for 30 min. Purified radiolabeled C4, C3, and C8 included in the complement source were bound to hemolysed SRC in direct proportion to the degree of hemolysis. These data indicate that polyclonal IgM-RF fix and activate complement via the classic pathway. The system described for assessing complement fixation by isolated RF is readily adaptable to use with whole human serum.

Animals↗