Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of in vitro indubation with gold sodium thiomalate (GST) on the morphology and functional activity of human mononuclear phagocytes (Mphi) was examined. Human peripheral blood Mphi that had been incubated with GST (25 micrograms/ml) for 4 days developed large intracytoplasmic vacuoles. Similar vacuolization developed after incubation with gold chloride but not with thiomalic acid. GST pre-incubation also induced a number of functional alterations in Mphi. GST incubation had little effect on glass adherence or FC receptor-mediated particle binding but markedly diminished pinocytosis of horseradish peroxidase and phagocytosis of IgG opsonized erythrocytes. These data indicate that the action of GST in rheumatoid arthritis may result from its capacity to alter the functional capability of Mphi.
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PMID:Alterations in human monocyte structure and function induced by incubation with gold sodium thiomalate. 11 43

A one-step sandwich enzyme immunoassay (EIA) for matrix metalloproteinase 3 (MMP-3; stromelysin-1) was developed. The assay system used two simultaneous immunoreactions using a solid phase monoclonal antibody and a horseradish peroxidase-labeled monoclonal antibody (Fab'). The sensitivity of the assay system was 20 micrograms/l and linearity was obtained between 31 and 500 micrograms/l. The EIA system was capable of measuring both precursor and active forms of MMP-3 as well as the forms of MMP-3 complexed with tissue inhibitors of metalloproteinases. MMP-3 levels as measured by this assay are significantly higher in the sera of patients with rheumatoid arthritis as compared to those of healthy subjects and patients with osteoarthritis. Immunoblot analyses showed that in the sera and synovial fluids of patients with rheumatoid arthritis, MMP-3 is present in the 59- and 57-kDa precursor forms.
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PMID:A one-step sandwich enzyme immunoassay for human matrix metalloproteinase 3 (stromelysin-1) using monoclonal antibodies. 128 63

Using a peroxidase/anti-peroxidase immunohistochemical staining method, we examined sections of inflammatory synovial membranes from 13 patients with juvenile rheumatoid arthritis (JRA) and 11 with rheumatoid arthritis (RA). The relative numbers of TCR gamma/delta+ cells and the proportions of V delta 1+ and V delta 2+ subsets were recorded in the areas of the membranes most heavily infiltrated by CD3+ cells. In the JRA group, the majority (8/13) of the membranes had TCR gamma/delta+ cells which contributed between 5 and less than 10% of the total number of CD3+ cells. In the RA synovial membranes examined, 5/11 samples had between 5 and 10% TCR gamma/delta+ cells, but in another 5 TCR gamma/delta+ cells contributed to between 10 and 20% of CD3+ cells. No significant difference was noted between the two patient groups. However, the range of values found in the RA membranes appeared to be slightly higher in comparison to previously reported values for RA synovial fluid, peripheral blood and eluted synovial membrane T cells. Analysis of the relative proportions of the V delta 1+ and V delta 2+ subsets revealed a significant dominance of V delta 1+ cells in RA membranes and approximately equal numbers of the two populations in the JRA patients. As the majority of peripheral blood TCR gamma/delta+ cells use the V delta 2 segment this suggests a preferential homing or expansion of the V delta 1+ cells in both RA and JRA synovium. The overall distribution pattern of the TCR gamma/delta+ and V delta 1+ and V delta 2+ cells was also recorded. These cells mostly accumulated in the lymphoid-like tissues and in the perivascular area in the tissues of both RA and JRA patients. Occasionally, augmented numbers of these cells were found in the subsynovial layer or in the loose connective tissue. In the majority of cases, only a few TCR gamma/delta+ cells were located in the synovial layer. The function and the possible pathogenetic importance of these TCR gamma/delta+ cells have not so far been determined.
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PMID:TCR gamma/delta+ cell subsets in the synovial membranes of patients with rheumatoid arthritis and juvenile rheumatoid arthritis. 141 Dec 99

The correlation between arthroscopic observations and histologic changes in rheumatoid arthritis is still controversial. Synovial samples of 21 knee joints in rheumatoid arthritis patients were comparatively investigated by endoscopy and histology. Biopsies were scored by an endoscopist and subsequently dissected. Different histochemical and immunocytochemical staining techniques were used to define inflammatory activity. Arthroscopic and histological values were compared by rating scales and variance analysis. Our study indicates that synovial biopsy is of diagnostic value in rheumatoid arthritis. However, its usefulness depends on the histochemical methods used. The results revealed highly significant correlations of endoscopic features with the number of neutrophilic granulocytes, intravascular leukocytes, and peroxidase-positive macrophages. However, no relationship was found between the detection of lymphocytes or resident macrophages and inflammatory scores. The close correlation between endoscopic and histological findings suggests that arthroscopic evaluation allows a valuable classification of the inflammatory activity in rheumatoid synovitis.
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PMID:Correlative histologic and arthroscopic evaluation in rheumatoid knee joints. 144 46

An inhibitor of myeloperoxidase has been identified in the synovial fluids and sera from patients with rheumatoid arthritis and sera from normal subjects. Initially, these fluids were found to inhibit stimulus induced degranulation of polymorphonuclear leucocytes independently of the stimulating agent. Subsequently, the fluids were shown to inhibit the released enzyme rather than the degranulation response of polymorphonuclear leucocytes. Both rheumatoid and normal serum samples contained high concentrations of the inhibitor but the concentrations were lower in rheumatoid synovial fluids. The inhibitory activity seemed to be specific for peroxidase as the fluids did not inhibit beta-glucuronidase activity. A protein of relative molecular mass (Mr) 150 kd was purified from synovial fluid by affinity chromatography on myeloperoxidase-Sepharose. It is concluded that serum and synovial fluid contain a novel myeloperoxidase inhibitor, which acts by binding to myeloperoxidase and thereby prevents myeloperoxidase releasing oxidative products in serum.
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PMID:Inhibition of myeloperoxidase by synovial fluid and serum. 164 55

Synovial tissue (ST) sections from patients with rheumatoid arthritis (RA) and meniscus lesions were stained using monoclonal antibodies against the carboxyterminal domain of human type I procollagen (alpha-pC) in avidin-biotin-peroxidase complex (ABC) staining. This gave a good signal-noise ratio and identified some synovial B-type lining cells and stromal fibroblasts in inflammatory RA ST but not in noninflammatory ST from patients with meniscus lesions. The authors' findings provide immunohistochemical evidence that the local fibroblasts in inflammatory ST in RA are activated, probably as a result of various humoral mediators produced in situ (by inflammatory mononuclear cells) in RA but not in normal noninflammatory ST.
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PMID:Fibroblasts in synovitis in rheumatoid arthritis but not in noninflammatory synovial tissue in meniscus lesions express the carboxyterminal domain of procollagen type I. 168 39

Previous evidence has been presented that neurogenic input may influence adjuvant induced arthritis (AA) in rats. We now present evidence of alterations in synovial nerves in AA. Nerves were studied in well perfused and fixed rats, using immunohistochemistry with the sensitive avidin-biotin peroxidase complex (ABC) method and heterologous antisera to cytoskeletal protein gene product 9.5 (PGP) and the neuropeptides substance P and calcitonin gene related peptide (CGRP). The innervation of synovium was compared in normal rats and rats with AA. Observations concordant with what has been reported for neuropeptide nerves in the synovium of patients with rheumatoid arthritis (RA) are presented. It has been suggested that neural peptide substances are reduced in nerves of synovium from patients with RA. In the AA rat a specific reduction of lining zone and sublining nerves in the synovium was noted. The AA rat model is very suitable for studying the involvement of synovial nerves in arthritis, permitting optimal preservation of immunoreactive neural epitopes.
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PMID:Nerves in inflammatory synovium: immunohistochemical observations on the adjuvant arthritis rat model. 170 59

46 patients with different rheumatic disorders were subjected to arthroscopic examination and the biopsied synovia were studied immunopathologically. Immunoglobulins, complements and fibrinogen deposition were detected by direct immunofluorescence, and rheumatoid factor (RF) deposition was detected by peroxidase-labelled denatured human IgG. Postoperative diagnosis of these cases were as follows: rheumatoid arthritis (RA) 21; seronegative spondylarthropathy 4; reactive arthritis 2; unidentified synovitis 4; osteoarthritis 8; and nonsynovitis conditions 5. It was shown that the positive rates of deposition of IgG, IgM, complement C3, C1q and C4, and RF in RA were 95.2%, 52.4%, 38.1%, 28.6%, 9.5% and 42.9%, respectively. Deposition was negative in all other rheumatic diseases. The positive fibrinogen deposition rate in RA was 42.9%; it was weakly positive in other disorders as well. The results indicate that the pathogenesis of RA is related to humoral immunity, and immunopathological study of the synovium has very important diagnostic significance in RA. On the other hand, deposition of fibrinogen lacks specificity for any rheumatic disease. The deposition of RF IgG, IgM and complement C3, C1q and C4 in the synovium of RA patients does not correlate well with clinical disease activity. The deposition of RF in the synovium also does not show paired correlation with blood IgM RF determination. This difference may be explained by the fact that the synovial RF examined in the present study may include all isotypes of RF and that hidden-RF in the blood may give a negative result. The synovium is the site of production of RF, but the degree of pathological change of the synovium of different joints in a single patient may not be uniform. The results of humoral immunity studies of the RA synovium may be influenced by the site selected for synovial biopsy.
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PMID:[Immunopathological study of synovium of rheumatoid arthritis]. 183 28

A monoclonal antibody and an affinity purified polyclonal antibody, both raised against recombinant human IL-6, have been employed in an ELISA procedure to quantitate human IL-6. Both antibodies were very potent in neutralizing the biological activity of recombinant as well as natural human IL-6. The monoclonal antibody was used as the capture antibody whilst the polyclonal antibody, in biotinylated form, was used as the detecting antibody in combination with a streptavidin horseradish peroxidase conjugate and a signal amplification system. The detection limit for natural as well as recombinant IL-6 was 1 pg/ml. A good correlation was found between the ELISA and the B9 biological assay when IL-6 was measured in crude culture supernatants, in synovial fluids of rheumatoid arthritis patients and in the sera of patients with diverse diseases. Immunoprecipitation of IL-6, produced by different cell types, such as monocytes, endothelial cells and smooth muscle cells or derived from biological fluids, such as the serum of a patient with septic shock or the synovial fluid of a rheumatoid arthritis patient, revealed in every case only molecules in the molecular weight range of 21,000-26,000.
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PMID:Sensitive ELISA for interleukin-6. Detection of IL-6 in biological fluids: synovial fluids and sera. 201 46

Using a monoclonal antibody directed against the C-chain of human C1q, we detected C1q-bearing immune complexes (IC) in sera and synovial fluids of rheumatoid arthritis (RA) patients. In a sandwich-ELISA, C1q-bearing IC were captured by the solid-phase monoclonal antibody and then detected with peroxidase-labeled F(ab')2-antibodies to either human IgG or IgM. The results of this assay were compared to an ELISA-modification of the C1q-solid-phase binding assay (C1q-SPBA). C1q-bearing IC were detected in 81.1% of RA-sera and the 65.2% of RA-synovial fluids. IgG as well as IgM was present in 72.6% of the sera and 70% of the synovial fluids which were positive in both assays. Most RA sera that were only positive for C1q-bearing IC, contained IgG alone (81.5%). The corresponding synovial fluids showed IgG alone (53%) or both IgG and IgM (41.1%). IgM alone (25%) could be detected in sera, e.g. in juvenile forms of RA. The levels of IC were higher in synovial fluid than in paired serum. In comparison to normal human serum (NHS) and patients with osteoarthritis, complement activity (CH50 titers) and C1q-values in patients with RA were frequently elevated. Since the formation of C1q-bearing IC is an indicator for the classical complement pathway activation, an assay with monoclonal anti-C1q antibody may be a useful tool in the diagnosis of rheumatoid diseases.
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PMID:C1q-bearing immune complexes detected by a monoclonal antibody to human C1q in rheumatoid arthritis sera and synovial fluids. 204 83


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