PubMed Health⌕ Search

Biomedical subjects

W J Koopman

Publications and source records attributed to W J Koopman.

At least 181 records · Page 10Linked to original sources
PubMed1984

Rheumatoid myositis. Clinical and histologic features and possible pathogenesis.

Thirty-one patients with rheumatoid arthritis were consecutively studied for evidence of muscle involvement, using muscle biopsy and electromyography. The patients were initially separated into 4 clinical categories: inactive peripheral joint disease (6 patients); active peripheral joint disease (10 patients); systemic disease and a disproportionately elevated sedimentation rate for the degree of mild synovitis (SERD) (11 patients); or elevated creatinine phosphokinase level (4 patients). In addition to routine histology, muscle tissue was examined for de novo synthesis of IgM and IgM rheumatoid factor, and by indirect immunofluorescence for the presence of immunoglobulin and complement deposits. Our results indicate that: muscle fiber necrosis occurs frequently in patients with rheumatoid arthritis; rheumatoid myositis, defined as muscle fiber necrosis and mononuclear cell infiltration, is a distinct entity and occurs particularly in patients with SERD or an elevated creatinine phosphokinase level; and only muscle from patients with rheumatoid myositis exhibited de novo synthesis of rheumatoid factor and significant quantities of IgM, indicating that local immune events may be important in the pathogenesis of this entity.

Arthritis, Rheumatoid↗
PubMed1984

Partial characterisation of the high and low molecular weight forms of P388D1-derived interleukin 1.

The murine macrophage-derived cell line P388D1 secretes the lymphokine interleukin 1 (IL-1) when stimulated by a variety of agents. When stimulated by bacterial lipopolysaccharide (LPS) the cells release IL-1 in both high and low molecular weight (m.w.) forms. The proportion of high m.w. IL-1 is reduced when IL-1-containing supernatants are concentrated by ammonium sulfate precipitation subsequent to hollow-fiber filtration. The high m.w. form can be converted to the low m.w. form by proteolysis, reduction and alkylation, or chromatography in a dissociating solvent. The low m.w. form remains as such, even when reconcentrated in fetal calf serum-containing medium. The high m.w. form thus likely consists of a complex between low m.w. IL-1 and another protein secreted by the P388D1 cell line.

Alkylation↗
PubMed1984

In vitro synthesis of IgM and IgM rheumatoid factor in seronegative arthritides.

In vitro patterns of IgM and IgM rheumatoid factor (RF) synthesis exhibited by peripheral blood B cells (MNL) obtained from healthy individuals as well as patients with seropositive and seronegative rheumatoid arthritis (RA) have been previously examined. The present study was performed in a group of patients with non-rheumatoid seronegative arthritis (SNA) in order to compare patterns of in vitro IgM and IgM RF synthesis to that previously observed with seropositive and seronegative RA. Eighteen patients with SNA (4 ankylosing spondylitis, 10 psoriatic arthritis, and 4 unclassified variant disease) were studied as well as 18 healthy adult controls. Spontaneous release of IgM RF by MNL was not observed in SNA or controls. In contrast, IgM RF was detected in pokeweed mitogen (PWM)-stimulated MNL culture supernatants from 9/18 SNA (mean +/- SD = 17.0 +/- 9.9 ng/10(6) cells), and 10/18 normal controls (16.7 +/- 9.9 ng). Synthesis of IgM by PWM-stimulated MNL from SNA (2062 +/- 1200 ng) was significantly less than observed with MNL from controls (4093 +/- 1896 ng) (P less than 0.001). There were no differences among the various SNA subsets with regards to the levels of IgM and IgM RF produced either spontaneously or after PWM stimulation. IgM RF constituted a small fraction of the total IgM in SNA and normals (0.9% and 0.5%, respectively). This is clearly distinct from seropositive RA in which we have previously established that IgM RF constitutes a substantial fraction of the total IgM (10.7%) (P less than 0.01). IgM and IgM RF production did not appear to be significantly influenced by immunosuppressive medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Penicillamine-induced myositis. Observations and unique features in two patients and review of the literature.

Dermatomyositis developed during treatment with penicillamine in two patients with rheumatoid arthritis. Both were male without a history of penicillin allergy. Eosinophilia was present at the start of their illness, and HLA tissue typing showed the presence of HLA-DR2 in one patient. One patient was retreated with penicillamine and remained asymptomatic after three years of therapy, and the other was able to take penicillamine in a reduced dosage.

Adult↗
PubMed1984

A unique precipitating autoantibody against plasma thromboplastin antecedent associated with multiple apparent plasma clotting factor deficiencies in a patient with systemic lupus erythematosus.

A 42-yr-old woman with systemic lupus erythematosus without bleeding diathesis developed a prolonged activated partial thromboplastin time that was not corrected by normal plasma. An inhibitor that acted rapidly and inactivated 0.5 U/ml plasma thromboplastin antecedent (PTA, factor XI) at a 1:200 plasma dilution was demonstrated. In addition to a low titer of PTA (less than 0.01 U/ml), plasma assayed at 20-fold dilution also showed low titers of Hageman (factor XII, 0.02 U/ml), Fletcher (plasma prekallikrein, 0.02 U/ml), and Fitzgerald (high molecular weight kininogen, less than 0.01 U/ml) factors. The titer of these factors, except PTA, returned to normal upon further plasma dilution or upon removal of the inhibitor by protein A adsorption. Thus, the inhibitor appeared to interfere with these clotting factor assays, possibly by inactivating PTA in the substrate plasmas in the test system. Its specificity was further confirmed. The inhibitor did not interfere with surface-induced proteolytic cleavage of Hageman factor. Surface-induced generation of plasma kallikrein activity (amidolysis of H-D-pro-phe-arg-pNa and cold-promoted factor VII activity enhancement) requires only Hageman, Fletcher, and Fitzgerald factors and was normal. Reactions requiring all 4 contact phase factors, including PTA, such as surface-induced generation of plasmin activity (amidolysis of H-D-val-leu-lys-pNa) and activated Christmas factor (factor IXa) activity, were defective. Furthermore, the inhibitor bound to agarose-protein A inactivated and removed PTA selectively from normal plasma. The inhibitor was an IgG-lambda autoantibody that precipitated PTA. The inactivated activated PTA (factor XIa) without the requirement for an additional cofactor. Furthermore, it inhibited surface-induced activation of PTA by interfering with its proteolytic cleavage upon glass surface exposure and with its binding onto the reactive surfaces.

Adult↗
PubMed1983

The IgA response: inductive aspects, regulatory cells, and effector functions.

In this review, we have emphasized our current studies on the inductive aspects of the IgA immune response and homeostatic mechanisms involved in the induction of oral tolerance. By use of unique inbred mouse strains in restricted microbial environments, we have provided evidence for a central role of LPS in systemic unresponsiveness to orally encountered antigens. We have continued studies on characterization of GALT lymphoreticular cell types, including accessory cells, regulatory T-cells, and precursor IgA B-cells. We have placed recent emphasis on characterization of antigen-specific Th-cell clones derived from murine PP, which preferentially support IgA isotype responses. Relevant areas for continued research have been emphasized in this review.

Animals↗
PubMed1983

Accessory cells in murine Peyer's patch. I. Identification and enrichment of a functional dendritic cell.

Previous studies have suggested that in vitro and in vivo immune responses are defective in Peyer's patch (PP) as a result of a deficiency in accessory cell number or function. However, we report here that enzymatic dissociation of PP does release a cell population with accessory activity in oxidative mitogenesis, i.e., the proliferation of periodate-modified T cells. The accessory activity present in PP is quantitatively similar to that of spleen. Accessory function is mediated by a cell type(s) that has the following characteristics: low buoyant density, lack of adherence to plastic or glass surfaces, lack of Fc receptors, and presence of surface Ia and the 33D1 dendritic cell (DC)-specific determinants. This PP accessory cell was markedly enriched by a novel technique. PP cells formed large aggregates when cultured for 16 h with irradiated, periodate-treated spleen cells. From the clusters we obtained a low density cell population that was 60% Ia positive, 33D1 positive, non-T and non-B, Fc receptor-negative, and dendritic in morphology. The DC-enriched populations were 60-80-fold enriched in accessory function relative to unfractionated PP. We can now compare PP accessory cells with accessory cells from other organs, and try to determine how PP dendritic cells contribute to the unique functions of this lymphoid organ.

Animals↗
PubMed1983

CREG antigens differentially influence expression of extraarticular manifestations in whites and blacks with rheumatoid arthritis.

B27 and the CREG antigens (-7, -27, -40, -42, and -22) have been shown to be related to the spondyloarthropathies. We have studied the frequency distribution of these antigens in patients with RA. Two hundred ninety-six patients with either classical or definitive RA by ARA criteria were studied: 199 were whites and 97 were blacks. Appropriate local control subjects were also studied (242 whites and 283 blacks). In the white RA patients 48.7% possessed a CREG antigen (97 of 199) while in the black patients 28.9% were CREG positive (28 of 97). In the white control subjects, 45.9% had a CREG antigen and 31.4% for the black control subjects. The relationship between CREG antigens and disease expression was compared using clinical, demographic, radiologic, and therapeutic parameters. For the white group there was no difference in the age and sex, disease duration, functional capacity, anatomic grading, C/M ratio, seropositivity, frequency of extraarticular manifestations (subcutaneous nodules, vasculitis, sicca symptoms, pleuropulmonary, or pericardial disease), frequency of remittive therapy, and toxicity to chrysotherapy. For the blacks all parameters were comparable except for a decrease in the frequency of extraarticular manifestations among the CREG-positive patients (21.4 vs. 46.4%) which is significant (p less than 0.05). Our data show no significant differences in the frequency of the CREG antigens in either blacks or whites with RA as compared to normal subjects. However, a possible sparing of some of the extraarticular manifestations of the disease appears to associate with the CREG antigens.

Arthritis, Rheumatoid↗
PubMed1983

Serum IgA1 and IgA2 in normal adults and patients with systemic lupus erythematosus and hepatic disease.

As an early step in examining the factors that regulate synthesis of the IgA subclasses, IgA1 and IgA2, we determined the serum levels of IgA1, IgA2 and total IgA in 50 normal adults, 20 patients with systemic lupus erythematosus (SLE), and 11 patients with liver disease. A quantitative solid phase radioimmunoassay using subclass specific monoclonal hybridoma antibodies was used. Within the normal population there were large variations in the concentrations of IgA1 and IgA2. The levels of IgA1 and IgA2 in samples from males were not significantly different from those from females. However, the mean concentration of IgA1 in samples from Blacks was significantly lower than that from Caucasians, P less than 0.005. In the control population IgA2 constituted from 6 to 35% of the total serum IgA and the levels of IgA1 did not correlate with the levels of IgA2. The mean IgA1 and total IgA in samples obtained from patients with SLE were significantly higher than those from the normal population (P less than 0.0001) although there was no significant difference in the levels of IgA2 in the two groups. In the samples obtained from patients with liver disease both IgA1 and IgA2 were markedly elevated and the levels of IgA1 did correlate with the levels of IgA2. These results indicate that the serum levels of IgA1 and IgA2 are controlled by factors that influence each subclass independently as well as factors that affect each subclass equivalently.

Adult↗
PubMed1983

Lymphoid cell responses to bacterial cell wall components: murine B-cell responses to a purified cell wall moiety of Actinomyces.

A mitogenic component, designated fraction C (Fr C), has been purified from a mutanolysin enzyme digest of Actinomyces cell walls by CM Sephadex C-25 ion-exchange and G-100 gel filtration chromatography. Good mitogenic responses were obtained with Fr C over a broad dose range with peak mitogenesis seen with 500 micrograms/culture. Fraction C (mol. wt. = 35,000-40,000) consists of 75% carbohydrate and 23% protein, is non-dialysable, resistant to heat, lysozyme or protease treatment, and partially sensitive to base, and all mitogenic activity is destroyed by either periodate or acid treatment. Fraction C is a B-cell mitogen since it induced responses in nude (nu/nu) and nu/+ BALB/c spleen cell cultures and purified splenic B-cell cultures, but did not stimulate purified splenic T-cell cultures. Similar mitogenic fractions for B cells have been obtained from cell walls of A. naeslundii and from a human isolate of A. viscosus. Good polyclonal IgM synthesis and plaque-forming cell responses to hapten or erythrocytes were obtained in vitro with the purified cell wall fractions derived from all three Actinomyces strains studied. These results indicate that the Actinomyces cell wall possesses a carbohydrate-rich component which activates B cells and may represent a common determinant of this genus.

Actinomyces↗
PubMed1983

Suppression of in vitro monoclonal human rheumatoid factor synthesis by antiidiotypic antibody. Target cells and molecular requirements.

Previous studies have indicated that antiidiotypic antibody can modulate expression of idiotype both in vivo and in vitro. Although the precise mechanisms underlying modulation of idiotype expression by antiidiotype remains unclear, a requirement for intact IgG antiidiotypic antibody has been suggested and T cells appear to play a role in some systems. We have studied peripheral blood mononuclear leukocytes (MNL) from a patient with a B cell lymphoma and a circulating IgMK rheumatoid factor (RF) paraprotein in an effort to delineate mechanisms involved in regulation of idiotype expression by antiidiotypic antibody. 1-10% of MNL from this patient could be cytoplasmically stained with specific F(ab')2 antiidiotypic antibody. MNL from the patient spontaneously synthesized IgM RF in culture that possessed the same idiotype as the circulating IgM RF paraprotein. Production of RF by MNL was suppressed by pretreatment with either intact IgG or the F(ab')2 fragments of antiidiotypic antibody (50% inhibitory concentration was 0.2 and 1.1 micrograms/culture, respectively). In contrast, the Fab' fragment of antiidiotypic antibody was not inhibitory (up to 57 micrograms/culture) despite retaining demonstrable antiidiotype activity. Suppression of RF production was not observed over the same concentration range with the IgG or F(ab')2 fractions of a non-cross-reactive antiidiotypic antibody prepared against another monoclonal IgMK RF paraprotein or with IgG or F(ab')2 fractions prepared from normal rabbit serum. Inhibition of RF production by antiidiotypic antibody did not require T cells. Antiidiotypic antibody decreased intracellular and extracellular levels of idiotype indicating diminished synthesis of idiotype by the patient's B cells. Synthesis of IgM RF by MNL obtained from unrelated donors was not suppressed by the antiidiotypic antibody specific for the patient's paraprotein. The results indicate that (a) antiidiotypic antibody is capable of directly suppressing human B cell release of idiotype, (b) the bivalent antigen-binding fragment (F[ab']2) of antiidiotypic antibody is sufficient for mediating such suppression, (c) an intact Fc portion of antiidiotypic antibody enhances suppression of idiotype, and (d) antiidiotypic antibody inhibits idiotype expression by suppressing synthesis of idiotype.

Animals↗
PubMed1983

DR antigen distribution in Blacks with rheumatoid arthritis.

DR antigen distribution was studied in 85 Blacks with either classical or definite rheumatoid arthritis (RA). Sixty-three were seropositive and 22 were seronegative by latex fixation titer. The frequency of DR4 was 7.41% in our control Black population (n = 162), 22.22% in the seropositive (0.01 greater than p greater than 0.001; RR 3.57) and 22.72% in the seronegative RA (0.01 greater than p greater than 0.001; RR 3.67). Our data confirm the association of DR4 with seropositive RA in Blacks, and suggest a similar association of DR4 with seronegative RA. It also suggests that DR4 may be a risk factor for more aggressive disease in Blacks with seropositive RA.

Black or African American↗
PubMed1983

Local synthesis of IgM and IgM rheumatoid factor in rheumatoid pleuritis.

Pleura from 3 patients with rheumatoid pleuritis and from 5 patients with other diseases was examined for its capacity to synthesize IgM and IgM rheumatoid factor (RF). IgM was synthesized by pleura from all 3 patients with rheumatoid pleuritis and IgM RF by 2. Pleura from each of the control patients synthesized less than or equal to 1 ng/mg of IgM and IgM RF. Moreover, pleura from a 4th patient with rheumatoid pleuritis incorporated 3H-leucine into newly synthesized IgM. Simultaneously obtained pleural fluid mononuclear cells (MNL) and pleural tissue from a patient with rheumatoid pleuritis synthesized identical proportions of IgM and IgM RF whereas IgM RF production was not observed with peripheral blood MNL from the same patient. The results support the view that local production of IgM and IgM RF occurs in rheumatoid pleuritis and suggest that local immune events contribute to the pathogenesis of this disorder.

Arthritis, Rheumatoid↗
PubMed1982

In vitro regulation of IgA subclass synthesis. I. Discordance between plasma cell production and antibody secretion.

To investigate the in vitro regulation of IgA subclass synthesis, peripheral blood lymphocytes from healthy adults were cultured with the polyclonal B cell activator, pokeweed mitogen. Although 50% of the IgA plasma cells from a 7-d culture were positive for cytoplasmic IgA1 and 50% were positive for IgA2, less than 10% of the IgA released into the culture supernatant was IgA2. This discrepancy could not be explained by failure of the assay to detect in vitro synthesized IgA2, selective loss or destruction of IgA2 in culture media, delayed release of IgA2, or failure of IgA2 plasma cells to produce J chain. The results suggest that additional signals may be required for the differentiation of plasma cells into immunoglobulin-secreting cells.

Adult↗