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Biomedical subjects

M Nobunaga

Publications and source records attributed to M Nobunaga.

At least 73 records · Page 4Linked to original sources
PubMed1990

The specificity of antiglobulin autoantibodies in patients with primary Sjögren's syndrome.

Antiglobulin autoantibodies have already been demonstrated in the sera of patients with primary Sjögren's syndrome (primary SS). In our study, the specificity of primary SS antiglobulins for different regions of IgG molecules was examined by employing both direct binding and competitive inhibition enzyme-linked immunosorbent assay. We found that a considerable amount of total antiglobulins in primary SS was specific for the Fab portion, although the remainder was specific for the Fc portion, namely rheumatoid factor (RF). In contrast, most of the antiglobulins in RA were specific for the Fc portion of IgG. These results indicate that in primary SS, antiglobulins directed against epitopes different from those of RF are produced. These antiglobulins may prove to have a different role in primary SS than that ascribed to RF in RA.

Antibodies, Anti-Idiotypic↗
PubMed1990

Rheumatoid factor modulation of neutrophil superoxide generation enhancing activity of preformed immune complexes.

Heat aggregated human (HAG) IgG pretreated with total rheumatoid factors isolated from the serum of rheumatoid arthritis patients showed decreased superoxide generation enhancing activity as compared with HAG pretreated with buffer alone. Similarly, monoclonal IgM rheumatoid factor isolated from the serum of a patient with macroglobulinemia complicated by rheumatoid arthritis inhibited superoxide generation enhancing activity of HAG. On the other hand, superoxide generation enhancing activity of BSA-antiBSA immune complexes was not affected by preincubation with rheumatoid factors isolated from the sera of either rheumatoid arthritis patients or the macroglobulinemia patient. Rheumatoid factors isolated from rheumatoid arthritis serum were fractionated by high performance liquid chromatography and IgM-class and IgG-class rheumatoid factors were obtained. IgG-class rheumatoid factor significantly enhanced the superoxide generation enhancing activity of HAG, whereas IgM rheumatoid factor inhibited it. Rheumatoid arthritis sera showed significantly higher superoxide generation enhancing activity than normal sera. HAG preincubated with rheumatoid arthritis sera showed significantly lower superoxide generation enhancing activity than HAG preincubated with normal sera. These results suggest that factors inhibiting superoxide generation enhancing activity of HAG are present in rheumatoid arthritis sera, and that the responsible is IgM rheumatoid factor, whereas IgG rheumatoid factor enhances it. The factors that express superoxide generation enhancing activity in rheumatoid arthritis sera are suggested to be intermediate size immune complexes.

Antigen-Antibody Complex↗
PubMed1990

Monocyte activation in early onset rheumatoid arthritis.

Monocytes from peripheral blood and synovial fluid of patients with definite and classic rheumatoid arthritis spontaneously produced significantly greater amounts of prostaglandin E2 (PGE2), leukotriene B4 (LTB4), and interleukin-1 beta (IL-1 beta) than samples of peripheral blood from normal controls. Peripheral blood monocytes from patients with rheumatoid arthritis produced significantly greater amounts of PGE2 than control samples when stimulated with lipopolysaccharide. There were no significant differences in the spontaneous release of superoxide or N-acetyl-beta-D-glucosaminidase by peripheral blood monocytes between patients and healthy controls. Both stimulated and unstimulated peripheral blood monocytes from patients with definite or classic rheumatoid arthritis produced significantly greater amounts of PGE2 than samples from normal controls. This was true, regardless of the stage of disease and the presence or absence of roentgenological joint abnormalities. Amounts of N-acetyl-beta-D-glucosaminidase released by peripheral blood monocytes from patients correlated positively with the erythrocyte sedimentation rate (ESR) and negatively with duration of disease. Amounts of IL-1 beta and N-acetyl-beta-D-glucosaminidase released from the peripheral blood monocytes of patients who had had their disease for less than one year were significantly higher than those of normal controls. There were no significant correlations between the types of treatment and the amounts of PGE2, LTB4, IL-1 beta or N-acetyl-beta-D-glucosaminidase released by peripheral blood monocytes in patients with rheumatoid arthritis. The findings suggest that monocytes are activated in patients with rheumatoid arthritis both at the onset of disease and during its chronic phase, and that they produce large amounts of mediators which may have a role in the induction and extension of the inflammatory process which leads to tissue damage.

Acetylglucosaminidase↗
PubMed1990

Antibodies to cytoskeletal systems in normal human serum.

Serum antibodies to cytoskeletal systems were measured by indirect immunofluorescence using human skin fibroblasts as the substrate for actin and vimentin, and HEp2 cells for cytokeratin. IgM concentration in 12 umbilical cord blood was less than 20 mg/dl, but antibody to cytokeratin was detected in samples that contained more than 10 mg/dl of IgM. Sera from 8-year-old pupils had elevated antibody titer to vimentin of IgG, IgM and IgA class and to cytokeratin of IgG and IgM class. Healthy adults had IgM anti-vimentin and anti-cytokeratin antibody at 60 times serum dilution, but other antibodies were lower than 10 times serum dilution. IgG and IgA concentration did not have any correlation with anti-cytoskeletal system antibodies. IgM concentration tended to correlate with IgM antibody titer to vimentin and cytokeratin. With increasing age in adults, antibody to actin of IgG class appeared.

Actins↗
PubMed1989

C1q binding to human vascular smooth muscle cells mediates immune complex deposition and superoxide generation.

Evidence was obtained for the binding of C1q to the membrane of cultured vascular smooth muscle cells derived from human umbilical cord veins. C1q was fixed to the cell membrane at 4 degrees C, whereas it was ingested into the cytoplasm, as a cytoplasmic inclusion, when tested at 37 degrees C. The addition of C1q in advance inhibited the subsequent binding of C1q. Neither fibronectin nor laminin was detected on the cell membrane. Aggregated IgG bound to vascular smooth muscle cells in the case of preincubation with C1q at 4 degrees C, whereas aggregated IgG did not bind to the cells in the absence of C1q. The addition of C1q molecules to the cells in suspension enhanced superoxide generation by vascular smooth muscle cells. There was no effect of C1q on superoxide generation by the cells in monolayer. These results suggest that C1q binds on the membrane of vascular smooth muscle cells via its specific receptor that mediates immune complex binding to the cells and superoxide generation. These properties elucidate the mechanisms by which circulating immune complexes deposit in the vascular wall, and subsequent degradation of tissue components surrounding vascular smooth muscle cells occurs through oxidative burst of the cells.

Antigen-Antibody Complex↗
PubMed1989

Iron-binding proteins and free iron in synovial fluids of rheumatoid arthritis patients.

Iron-binding proteins (lactoferrin, transferrin and ferritin) and free iron were measured in synovial fluid (SF) from 30 patients with rheumatoid arthritis (RA) and 20 osteoarthritis (OA) patients. The iron-binding proteins except transferrin were significantly increased in RA SF as compared with OA SF. Similarly, free iron was also significantly higher in RA SF than in OA SF, whereas the ferritin saturation index, transferrin saturation index and bound iron were more significantly decreased in RA SF than in OA SF. These results suggest that RA SF contains sufficient micromolar amounts of free iron to allow hydroxyl radical formation. Also the capacity of iron-binding proteins to bind free iron is inadequate in the presence of a large amount of iron-binding proteins which are present in RA SF.

Antigen-Antibody Complex↗
PubMed1989

Possible role of H2O2-mediated complement activation and cytokines-mediated fibroblasts superoxide generation on skin inflammation.

The degree of complement activation produced by hydrogen peroxide was estimated by the inhibition of serum homolytic activity (% IHA). Sera from patients with systemic lupus erythematosus and psoriasis vulgaris were resistant to hydrogen-peroxide-mediated complement activation. %IHA negatively correlated with ceruloplasmin level or catalase activity in systemic lupus erythematosus sera, but did not correlate with transferrin level. The addition of free metal ions, FeCl2 or CuCl2, promoted hydrogen-peroxide-mediated complement activation. These results suggest that hydroxyl radical is involved in complement activation and that the factors responsible for the insensitivity of pathological sera to H2O2 are catalase and ceruloplasmin in the sera. Human skin fibroblasts generate superoxide and tumor necrosis factor enhanced it, but interleukin-1 beta inhibited it. Normal serum cultured with fibroblasts for 24 h showed complement activation via catalase-inhibitable process, suggesting that hydrogen peroxide has an important role in fibroblast-mediated complement activation. It is speculated that fibroblasts and complement activation by oxygen radicals have an important role in inflammation and subsequent tissue damage at the site of skin lesion.

Cells, Cultured↗
PubMed1989

[Proposal of revised criteria for malignant rheumatoid arthritis].

The diagnostic criteria for malignant rheumatoid arthritis (MRA), which was proposed by the Research Group of MRA and periarteritis nodosa supported from the Ministry of Health and Welfare has been widely used since 1973. This diagnostic criteria was established for selecting RA patients with life-threatening extraarticular manifestations caused by vasculitis. However, in practice, RA patients with extraarticular involvements related to vasculitis, as well as, cases which were not related to vasculitis were diagnosed as MRA in this criteria. Because of the aforementioned and after research, we revised the diagnostic criteria for MRA. At first, we defined MRA as RA patients having intractable and severe extraarticular manifestations by various causes including vasculitis. One hundred and sixty-nine patients with MRA and 227 patients with RA from 39 medical facilities were analysed. Sixteen extraarticular clinical manifestations and 9 laboratory findings were compared between MRA and RA patients. Comparison of specificity in each criterion for MRA was made by using the Second quantitative analysis. Thereafter, the combinations of the variables which were most specific to MRA were studied. At the same time, sensitivity and specificity for MRA were also studied. The revised criteria are as follows: A. Clinical and Laboratory Findings--(1) visceral infarction, (2) myocarditis, (3) skin ulcer or skin infarction, (4) episcleritis or iritis, (5) polyneuritis, (6) high titers of rheumatoid factor, (7) immune complexes or low complement levels, (8) subcutaneous nodule, (9) pleuritis or pericarditis, (10) interstitial pneumonitis or lung fibrosis. B. Histopathological Findings from Biopsy Specimens--necrotizing vasculitis and/or granulomatous vasculitis and/or endoarteritis obliterans in small and/or medium size arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗
PubMed1989

Multiple rheumatoid bursal cysts.

We have encountered a patient with rheumatoid arthritis (RA) who developed multiple subcutaneous swellings containing sterile milky fluid. The resected material showed chronic granulomatous changes compatible with rheumatoid inflammation. We suggest that multiple chronic rheumatoid inflammation may occur in the bursae as well as joint synovium as one of the extraarticular manifestations of RA.

Arthritis, Rheumatoid↗
PubMed1989

[Evaluation of disease activity by hand X-ray findings in rheumatoid arthritis].

It would appear to us that the patients with rheumatoid arthritis (RA), in whom articular bone lesions were confined to the wrist and/or carpal joints in X-ray films, may follow a milder disease activity than do the patients with the hand and finger joint lesions. To clarify it, the present study was performed retrospectively. RA patients showing stage II or more lesions in the wrists and/or carpal joints but no lesions over stage II in any hand and finger joint (MCP, IP and PIP) radiologically after 5 years or more duration were regarded as the carpal type (C type). The clinical and laboratory data were compared between 44 patients of the C type RA and 44 patients of other type RA, matched in the sex, age and disease duration. Significant differences were observed in the following parameters between the 2 groups; the functional class, Lansbury's activity index, number of the affected joints, ESR, CRP and hemoglobin values, and ADL scores. That is, Hb values and ADL scores were higher, but the others were lower, in the C type RA group than in other type RA group. The positive percentage and titer of rheumatoid factor were not significantly different between the 2 groups. It was concluded that C type RA patients are milder in the activity and fewer in the number of affected joints than other type RA patients. Furthermore it was suggested that C type RA patients may have milder clinical course and better prognosis than other type RA patients.

Adult↗
PubMed1989

[Antibodies to cytoskeletal systems in patients with adult T-cell leukemia and infectious mononucleosis].

Serum antibodies to cytoskeletal systems were measured by indirect immunofluorescence using human skin fibroblasts and HEp2 cells as substrate. Healthy adults had IgM antibodies to vimentin and cytokeratin at 60 times serum dilution. IgG concentration did not have a correlation with IgG anti-cytoskeletal system antibodies and IgM concentration correlated with anti-vimentin and anti-cytokeratin antibodies. In patients with adult T-cell leukemia (ATL), IgG antibody titer against actin and vimentin was increased in spite of a decreased IgG concentration. IgM antibodies to vimentin was decreased in its titer together with a decreased IgM concentration. Antibody titer to HTLV-1, leukemic cell counts in peripheral blood and disease type, acute or chronic, did not have correlations with anti-cytoskeletal system antibodies. A third of the patients with ATL showed negative anti-EBNA antibody, suggesting that the functional impairment in EBV-specific killer cells was present. In contrast, the patients with infectious mononucleosis showed increased serum IgM concentration and IgM anti-vimentin antibody titer. It was suggested that the autoantibodies to cytoskeletal systems associated with viral infection were mainly composed of IgG in ATL and of IgM in infectious mononucleosis.

Adult↗
PubMed1988

Complement-activating properties of immune complexes are suppressed by IgM rheumatoid factor and enhanced by IgG rheumatoid factor.

The effect of rheumatoid factor (RF) on complement-activating capacity of aggregated IgG was investigated. The degree of complement activation induced by the addition of specific amounts of aggregated IgG to patients' sera and normal sera was demonstrated by the inhibition of hemolytic activity (%IHA). The %IHA was significantly lower in rheumatoid arthritis (RA) sera and higher in systemic lupus erythematosus (SLE) sera, compared with normal sera. There was a negative correlation between %IHA and IgMRF/IgGRF ratio in RA and SLE sera, and RA synovial fluid. The %IHA and IgGRF were positively correlated in RA sera. The IgMRF/IgGRF ratio was significantly lower in SLE sera than in RA sera and systemic sclerosis sera, and was significantly lower in RA synovial fluid than in osteoarthritis synovial fluid. Isolated RF, consisting of mostly IgMRF class, inhibited complement-activating properties of aggregated IgG, depending on the concentration of RF. Isolated RF was further purified by the fractionation using high pressure liquid chromatography, and IgGRF and IgMRF were obtained. IgMRF significantly suppressed the complement-activating capacity of aggregated IgG, whereas IgGRF promoted it. These observations suggest that IgMRF acts protectively, while IgGRF induces inflammation. Thus, the expression of the biological activity of RF with special reference to immune complex interaction mainly depends on the IgMRF/IgGRF ratio.

Antigen-Antibody Complex↗