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W J Koopman

Publications and source records attributed to W J Koopman.

At least 163 records · Page 9Linked to original sources
PubMed1986

Induction of neutrophil enzyme release by rheumatoid factors: evidence for differences based on molecular characteristics.

Cathepsin G and elastase are two neutrophil proteases capable of degrading the major structural macromolecules of the joint. Evaluation of factors capable of inducing the release of these enzymes is crucial to the understanding of neutrophil-mediated tissue destruction. We have evaluated the effects of IgM rheumatoid factor (RF), as well as monomeric and polymeric forms of IgA RF, on the release of neutrophil elastase, cathepsin G, and the specific granule protein lactoferrin. None of these rheumatoid factors alone was able to induce more lysosomal protein release than media controls. Under conditions used in this study, aggregated human IgG was able to induce slightly more release than media controls. The addition of IgM RF or polymeric IgA RF to the aggregated IgG resulted in release of significantly more lysosomal proteins than aggregates alone. In contrast, monomeric IgA RF, even in the presence of aggregated IgG, was unable to augment enzyme release. These results suggest that differences in the molecular characteristics of RF found in synovial fluid may significantly influence the contribution of RF to tissue injury in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1986

Interleukin 1-like factor produced by a hybrid of an adherent mouse spleen cell and a thymoma cell.

A hybrid cell line (DCH-5) constructed from an adherent cell of mouse spleen and the thymoma BW5147, and selected for adherence to hydrophobic surfaces, secretes a factor which augments the mitogenic response of thymocytes. Properties of the factor were compared with those of a P388D1 and J774.1 macrophage-derived interleukin 1 (IL-1). On polyacrylamide gel electrophoresis in Tris-glycinate buffer the IL-1-like factor of DCH-5 cells was heterogeneous and its components were more negatively charged than components of macrophage-derived IL-1. Charge differences between these factors were also confirmed by isoelectric focusing (IEF) (pI of IL-1 was 5.4, pI of the IL-1-like factor was 3.5). SDS-PAGE and gel filtration demonstrated that both factors consisted of several components of near molar masses (approximately 17 kg/mol). Gel filtration showed that in PBS the IL-1-like factor of DCH-5 cells was partially aggregated. Antibodies specific to IL-1 inhibited the activity of the IL-1-like factor of DCH-5 cells. Thus, mouse DCH-5 cells provide a new source of IL-1-like factor which might be useful for further elucidation of the heterogeneity of interleukins.

Animals↗
PubMed1986

Circulating immune complexes and immunoglobulin A rheumatoid factor in patients with mesangial immunoglobulin A nephropathies.

Circulating immune complexes (CIC) containing IgA and C3 were elevated in 48% of IgA nephropathy patients; IgA1 was the predominant subclass. IgA1-IgG CIC were detected in 44%, IgA2-IgG CIC in 7%, and IgM-IgA1 CIC in 16% of the patients. No IgM-IgA2 CIC were detectable. Sucrose gradient ultracentrifugation indicated that IgG-IgA1 CIC were predominantly of intermediate (13-19S) size whereas IgA1-C3 CIC sedimented from 11S to 19S. At acid pH, isolated CIC revealed the presence of substantial amounts of 7S IgA. One third of the patients had elevated serum IgA rheumatoid factor (RF) of both polymeric and monomeric forms despite normal levels of IgM-RF; 87% of patients with elevated IgA-RF had IgA1-IgG CIC. These results indicate that the IgA1 component of CIC in patients with IgA nephropathy is not necessarily of mucosal origin and suggest that a portion of these CIC consists of IgA RF immunologically complexed with autologous IgG.

Antigen-Antibody Complex↗
PubMed1986

Rheumatoid arthritis associated with expanded populations of granular lymphocytes.

Two patients with classic rheumatoid arthritis developed severe neutropenia and increased numbers of large granular lymphocytes in the blood and bone marrow. These lymphocytes exhibited homogeneous surface membrane immunophenotypes of Leu5+, Leu11-, Leu4+, Leu3-, Leu2-, Leu7+ and Leu5+, Leu11+, Leu4+, Leu3-, Leu2+, Leu7-, respectively. In both patients, neutropenia was initially corrected with corticosteroid therapy; long-term improvement followed low-dose oral cyclophosphamide and methotrexate therapies. In these 2 patients and 12 previous patients with rheumatoid arthritis associated with expanded populations of immunophenotypically homogeneous large granular lymphocytes, neutropenia occurred in all 14, thrombocytopenia in 6, anemia in 7, and mild or moderate splenomegaly in 12. In contrast to Felty's syndrome, granular lymphocyte expansions in rheumatoid arthritis usually occur in older patients, may appear simultaneously with arthritis, and are usually associated with normal or elevated blood leukocyte counts. Mild hemocytopenias in these patients can often be managed with observation. Therapy with corticosteroids or immunosuppressive-cytotoxic drugs may be beneficial in more severe cases, but splenectomy is not recommended.

Aged↗
PubMed1985

Etiopathogenesis of the rheumatoid arthritis-like disease in MRL/l mice. I. The histomorphologic basis of joint destruction.

MRL/l mice spontaneously develop a hindlimb arthropathy, as well as a number of immunologic abnormalities, including circulating rheumatoid factors. Although previous studies have suggested that this arthropathy is primarily an inflammatory process, we performed a comprehensive histomorphologic study which indicated that inflammation is a late manifestation of MRL/l arthritis. The pathologic changes that occur in the joints of these mice can be divided into 3 stages. The first stage develops between the ages of 7 and 13 weeks and consists of synovial cell proliferation in the joint recesses. The second stage is characterized by continued proliferation of synovial cells which take on an appearance similar to that of transformed mesenchymal cells. The earliest destructive changes occur in the second stage and include marginal erosions, followed soon after by progressive destruction of articular and meniscal cartilage. The final stage is characterized by a diminution of synovial cel proliferation, extensive cartilage destruction, formation of scar tissue and fibrocartilage, and a very moderate infiltration of the synovial stroma by mononuclear and polymorphonuclear inflammatory cells. Throughout the disease progression there is a striking dissociation between inflammatory cell infiltration or exudation and tissue destruction. The histomorphologic similarities between human rheumatoid synovitis and the arthritis of MRL/l mice, as well as the presence of rheumatoid factors, make this mouse strain an excellent model for studying human rheumatoid arthritis.

Animals↗
PubMed1985

IgA rheumatoid factor synthesis by dissociated synovial cells. Characterization and relationship to IgM rheumatoid factor synthesis.

We examined patterns of IgA rheumatoid factor (RF) and IgM-RF synthesis by dissociated synovial cells obtained from 27 patients with seropositive rheumatoid arthritis. Synthesis of IgA-RF was observed in 19 of 34 synovial cell preparations from these patients and constituted a mean of 16% of the total IgA produced. IgA-RF expression correlated only weakly with IgM-RF production (r = 0.385) and could be dissociated from production of IgA-RF (and IgM-RF) exhibited by simultaneously obtained peripheral blood plasma cells. While wide variations were observed in the ratio of IgA-RF:IgM-RF produced by synovial B cells in the patient sample studied, remarkable consistency in the relationship of IgA-RF to IgM-RF synthesis was observed over time in different joints of the same patient. IgA-RF synthesized by dissociated synovial cells was predominantly of the IgA1 subclass and existed in both monomeric and polymeric forms. Our results are compatible with the view that local production of IgA-RF and IgM-RF are regulated independently of each other.

Adult↗
PubMed1985

Solid-phase radioimmunoassay for human neutrophil elastase: a sensitive method for determining secreted and cell-associated enzyme.

A solid-phase radioimmunoassay for measuring neutrophil elastase in the range 0.08-4 ng/ml has been developed. A monospecific, precipitating antibody capable of inhibiting elastinolysis was produced by repeated immunizations of a goat. The IgG fraction and affinity-purified antibodies of this serum were then obtained and used to develop this radioimmunoassay. There was no cross-reactivity in binding of the radiolabeled antisera with lactoferrin, cathepsin G, or serine proteinases with amino-terminal amino acid sequence homology. Although serum influences the measurement of catalytically active neutrophil elastase when compared to diisopropylfluorophosphate-treated neutrophil elastase, antigenic elastase may still be measured in body fluids. Furthermore, this assay is more sensitive than commercially available substrates used for quantitating neutrophil elastase by functional activity. We have found this quantitative assay extremely useful in balance studies to measure secreted and cell-associated elastase and in screening of biological fluids for the presence of the enzyme.

Animals↗
PubMed1985

Immunoglobulin subclass distribution of synovial plasma cells in rheumatoid arthritis determined by use of monoclonal anti-subclass antibodies.

The distribution of IgG and IgA subclass plasma cells among dissociated synovial cells from 14 rheumatoid arthritis (RA) synovia was examined by immunofluorescence using mouse monoclonal anti-human subclass antibodies. Of the IgG plasma cells 81 +/- 9% were IgG1, 4 +/- 2% IgG2, 14 +/- 9% IgG3, and 0.9 +/- 0.6% IgG4. While IgG1 predominated in all 14 synovia (which is similar to what is seen in normal tissues), in 5/14 20% or greater of IgG plasma cells were IgG3, suggesting a selective increase in IgG3 production in the synovia of certain RA patients. Among IgA plasma cells 89 +/- 5% were IgA1 and 8 +/- 3% were IgA2. This distribution is similar to the distribution in normal serum.

Antibodies, Monoclonal↗
PubMed1985

Activity of rheumatoid factors of different molecular sizes: comparison of autologous monomeric and polymeric monoclonal IgA rheumatoid factors.

Differences in rheumatoid factor (RF) activity among the molecular species of IgA were investigated with the use of monomeric and polymeric monoclonal IgA RF paraprotein from the serum of a patient (PS) with idiopathic hyperviscosity syndrome. After fractionation by gel chromatography in acidic buffer, RF activity as determined by latex fixation and solid-phase radioimmunoassay (RIA) specific for IgA RF was confined to the high m.w. (greater than 7S) fractions. However, after adsorption into polystyrene wells, fractions containing monomeric (7S) IgA, as well as those containing polymeric IgA, bound 125I-labeled heat-aggregated human IgG. These observations were confirmed after further purification of the IgA fractions by passage through a protein A-Sepharose CL-4B column followed by precipitation of the IgA proteins with ammonium sulfate at 50% saturation. After "cross-linkage" by a hybridoma anti-human alpha-chain antibody, the activity of the monomeric IgA preparation in the IgA RF RIA approached that of the polymeric IgA preparation. Gel filtration studies verified that this activity was not due to contamination by polymeric IgA RF. Further, classic RF specificity was confirmed for both the monomeric and polymeric IgA RF by reaction with human Fc-coated but not Fab-coated wells. A control monomeric IgA myeloma protein and normal serum IgA did not react in the RF RIA when analyzed in the presence or absence of the hybridoma anti-alpha-chain antibody. Moreover, the activity of the polymeric IgA RF preparation from patient PS in the RIA was minimally influenced by the hybridoma antibody. These results indicate that IgA RF can coexist in both polymeric and monomeric forms, demonstrate that monomeric IgA RF may escape detection by previously described RIA techniques, and suggest an approach for its detection.

Animals↗
PubMed1985

Interaction of DNA with connective tissue matrix proteins reveals preferential binding to type V collagen.

The interaction of DNA with type I to VI collagens and laminin was studied in vitro in systems in which the connective tissue components were immobilized, as well as when in solution. In studies on immobilized components, significant binding of DNA was observed only for type V collagen, and the binding of radiolabeled DNA to this component could be effectively inhibited in a concentration-dependent manner by the addition of unlabeled DNA. Similar results were observed in solution assays in which it was observed that DNA binding to type V collagen was dependent on the native triple-helical conformation of the collagen. The preferential binding of DNA to native type V collagen may be due to the relative basicity of type V collagen chains, as well as the unique spatial arrangement of amino acid side chains in the native molecules. The data are of potential clinical relevance in that binding of DNA to type V collagen may represent at least one component of the mechanism whereby DNA and its immune complexes are deposited in connective tissues in certain pathologic conditions.

Animals↗
PubMed1985

The carpometarcarpal ratio: a useful method for assessing disease progression in rheumatoid arthritis.

Determining the progression of anatomic involvement in rheumatoid arthritis (RA) is a well recognized problem. In 1976, Trentham and Masi described the carpometacarpal (CMC) ratio and found it useful for detecting progression of anatomic involvement in RA. Our study attempts to validate the efficacy of this ratio both in a cross sectional (n = 267) and longitudinal (n = 53) sample of patients with rheumatoid arthritis. Our data indicate that the CMC ratio is useful for quantitating anatomic involvement and correlates well with anatomic progression over time.

Arthritis, Rheumatoid↗
PubMed1984

Preferential induction of polyclonal IgA secretion by murine Peyer's patch dendritic cell-T cell mixtures.

Polyclonal IgA secretion is inducible in murine B cells when DC-T from Peyer's patches (PP) provide the inducing stimulus. PP DC-T, which are composed predominantly of dendritic cells and Lyt-1+ T cells, are capable of dramatic augmentation of IgA secretion by PP or spleen B cells with minimal induction of IgM secretion. DC-T from spleen, however, are incapable of augmenting IgA secretion by either PP or spleen B cells. The level of IgA secretion is dependent upon the dose of DC-T providing the inducing stimulus and reaches a plateau with DC-T:B ratios of less than 1:1. This system for preferential induction of IgA responses should permit elucidation of cellular mechanisms involved in regulation of IgA secretion.

Animals↗
PubMed1984

Isotype specificity of helper T cell clones. Peyer's patch Th cells preferentially collaborate with mature IgA B cells for IgA responses.

The nature of the IgA B cell precursors that receive preferential help from selected clones of T helper cells from mouse Peyer's patches (PP Th A) were studied. Activation of the PP Th A clones required the presence of antigen, sheep erythrocytes (SRBC), in a culture system supporting development of antibody-secreting plasma cells. Two types of PP Th A cells were used. Both gave vigorous IgA responses; the first also supported low IgM, and the second low IgM and IgG subclass antibody responses. Removal of sIgA+ B cells from either splenic or PP B cell cultures selectively depleted precursors of IgA antibody producers. Cultures of purified sIgA+ B cells, cloned PP Th A cells and SRBC, selectively yielded IgA antibody producers. Finally, PP Th A cells did not support IgA responses in B cell cultures derived from spleens of young mice (days 1-25), and full IgA responses were not seen until the donor mice were 6-7 wk of age. These results suggest that cloned T helper cells can recognize and collaborate with mature, IgA committed B cells.

Animals↗
PubMed1984

DR antigens and gold toxicity in white rheumatoid arthritis patients.

An increase in the frequency of DR3 in rheumatoid arthritis (RA) patients exhibiting toxic reactions to chrysotherapy has been reported in several studies of white patients. This study was designed to compare DR antigen frequencies in local white RA patients undergoing chrysotherapy with their response to treatment. The results from our sample of RA patients (n = 148) confirm the fact that there is increased frequency of DR3 in patients who develop toxic reactions to gold therapy, as reported in other studies of white patients. The DR3 increase was attributable to those gold-treated patients who developed proteinuria, and was not observed in patients who developed skin toxicity. Interestingly, the associations were not as strong as those found in other reports. Only 21.1% of the patients with DR3 manifested toxic reactions overall, with only one-third of the patients with proteinuria being DR3 positive. There was also an association of toxicity, albeit not significant, with a decreased frequency of DR2, which is consistent with the suggestion that this phenotype may protect against adverse reactions to gold treatment. These results suggest that while DR3 is significantly associated with adverse response to gold treatment, the relationship is not as strong as that previously reported. Explanation of these differences remains to be elucidated.

Arthritis, Rheumatoid↗