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Biomedical subjects

M R Daha

Publications and source records attributed to M R Daha.

At least 289 records · Page 16Linked to original sources
PubMed1990

Significance of rheumatoid factor isotypes in seronegative rheumatoid arthritis.

In a cross-sectional study of 124 patients with definite or classical rheumatoid arthritis (RA) and negative agglutination assays, rheumatoid factor (RF) isotypes were measured using an ELISA technique. Elevated levels of IgA-RF were found in 55 patients (44%), IgG-RF in 99 (80%), and IgM-RF in 20 (16%). The levels of IgA- and IgM-RF correlated with each other (P less than 0.001). Elevated levels of IgM-RF were associated with a more severe disease course. Elevated levels of IgA-RF correlated with the occurrence of bone erosions. The results of this study suggest that in patients with RA and negative agglutination assays, both IgM- and IgA-RF are markers of disease severity.

Adult↗
PubMed1990

Rat polymeric IgA binds C1q, but does not activate C1.

Immune complexes, prepared with monoclonal rat IgA antibodies directed against DNP, activate the alternative pathway of the complement system in rat serum. In this study, the interaction of these monoclonal IgA antibodies with the classical pathway of complement was investigated. Monoclonal polymeric IgA (p-IgA) was shown to inhibit the IgG2b-mediated classical pathway-dependent lysis of TNP-coated sheep red blood cells. In addition, the binding of C3 to solid phase IgG2b immune complexes was inhibited by p-IgA. Monoclonal monomeric IgA (m-IgA) was much less efficient in this respect. To further analyse the effect of p-IgA on the activation of the classical pathway by IgG2b immune complexes, the interaction of p-IgA with C1 was studied. It was found that p-IgA antibodies bind C1q. No species-specificity was observed, since both rat and human C1q were bound. Whereas binding of C1q in C1 to IgG2b resulted in activation of C1, binding to p-IgA did not. The binding of C1q to both p-IgA and IgG2b could be inhibited by monoclonal antibodies directed against the globular heads of C1q, but not by monoclonal antibodies directed against the collagen tail. The formation of insoluble p-IgA immune complexes was inhibited in the presence of rat serum or C1. These studies indicate that C1q binds to p-IgA by its globular heads, and thereby may modulate classical pathway-mediated reactions such as the inhibition of immune precipitate formation.

Animals↗
PubMed1990

Renal allograft-infiltrated lymphocytes and proximal tubular cells: further analysis of donor-specific lysis.

We obtained both graft-infiltrating cells of host origin and proximal tubular epithelial cells (PTEC) of donor origin (using a selective serum-free medium) simultaneously from biopsies of rejecting renal allografts. The identity of PTEC cultures was established with monoclonal antibodies. Major histocompatibility complex class I expression could be upregulated and major histocompatibility complex class II expression induced on PTEC by 24- to 48-hr incubation with 200 U interferon-gamma. Graft-infiltrating cells were shown to lyse PTEC grown from the corresponding biopsy and not PTEC from biopsies from other patients. Therefore the lytic activity appeared to be donor-specific. Preincubation of PTEC with interferon-gamma did not consistently increase PTEC lysis. Lysis by graft-infiltrating cells obtained from four patients could be blocked by target-preincubation with anti-class I monoclonal antibodies, in one case both anti-class I and anti-class II monoclonal antibodies could block PTEC lysis. Blocking could also be obtained with anti-CD3 monoclonal antibody. PTEC lysis occurred only with graft-infiltrating cells cultured from biopsies with cellular interstitial rejection. So, PTEC seem to be a target in renal allograft rejection both in vivo and in vitro. This model system may be useful for further studies of cellular interactions between graft-infiltrating cells and their targets.

Adult↗
PubMed1990

Degradation of aggregates of activated C3 (C3b) by monocytes of patients with rheumatoid arthritis is related to vasculitis.

We investigated whether a decreased complement receptor expression or function of monocytes isolated from peripheral blood of 52 patients with rheumatoid arthritis (RA) and rheumatoid vasculitis (RV) could account for the previously observed diminished degradation of immune complexes by monocytes of patients with RA and RV. On average, monocytes from all patients expressed significantly less CR1, and degraded significantly less AC3b when compared with monocytes of healthy controls. In addition, monocytes from RV patients degraded significantly less AC3b when compared with monocytes from patients with RA. The expression of both CR1 and CR3 on monocytes of RV patients was lower compared with RA patients but this difference was only significant for CR3. No differences were found between AC3b degradation and the expression of CR1 and CR3 between patients with active and inactive RA. Using linear discriminant analysis on the variables AC3b, CR1 and CR3, 94% of the patients could be classified correctly as healthy controls, RA or RV, suggesting a true multi-variate relationship between these parameters and patients groups. Our results suggest that the diminished capacity of monocytes from RA patients to degrade AC3b is due partly to a decreased expression of CR1 and CR3.

Adult↗
PubMed1990

Cytolytic activity in T cell clones derived from human synovial rheumatoid membrane: inhibition by synovial fluid.

A panel of T cell clones was derived from the synovial membrane of a patient with rheumatoid arthritis (RA). We investigated whether T cell clones with cytolytic properties were present and whether T cell cytotoxicity was influenced by the presence of synovial fluid. These issues were studied using anti-CD3 and lectin-induced cytotoxicity assays. The majority of the T cell clones derived from the synovial membrane showed cytotoxic properties although non-cytotoxic clones were also found. Three clones (N11, N6 and N15) showed strong cytotoxicity (more than 40% lysis at an effector-to-target cell ratio of 10:1) whereas three clones (N16, N4 and N14) were non-cytotoxic (less than 20% lysis at an effector-to-target cell ratio of 10:1). The induction of cytotoxicity in the anti-CD3-driven system was shown to be dependent on the dose of anti-CD3 present. When synovial fluid was added to these assays a strong inhibition of cytotoxicity was found. This inhibition of cytotoxicity was found with synovial fluid samples of RA patients, as well as with non-RA synovial fluids. Both anti-CD3 and lectin-dependent cytotoxicity assays were strongly inhibited. In conclusion, T cell clones with cytotoxic activity can be isolated from rheumatoid synovial membrane. In the presence of synovial fluid these cytotoxic cells are inhibited to exert their cytotoxic function.

Antibodies, Monoclonal↗
PubMed1990

Dominant T-cell receptor beta-chain gene rearrangements indicate clonal expansion in the rheumatoid joint.

T-cell receptor (TcR) beta and delta gene rearrangements were studied in anti-CD3 expanded T-cell populations cultured from the synovial membrane (SM) (n = 5) or synovial fluid (SF) (n = 2) of rheumatoid arthritis (RA) patients. Dominant TcR beta-chain gene rearrangements to C beta 1 were demonstrated in all the patients tested and 1-3 expanded clones per patient were found. Clonal rearrangements to C beta 2 were detected in one SM sample (two clones) and one SF sample (one clone). The TcR delta gene was deleted in all the samples tested. We conclude that clonal dominance may be found in expanded T-cell populations from SM and SF of RA patients. Multiple clones may be present, either using the C beta 1 or C beta 2 gene segment.

Adolescent↗
PubMed1990

The involvement of Kupffer cells in the clearance of high molecular weight rat IgA aggregates in rats.

In the present study the clearance kinetics and tissue distribution of aggregated 125I-labelled monoclonal rat IgA [( 125I] AIgA) of different sizes were studied in rats. Soluble [125I]AIgA disappeared from the circulation in a biphasic manner with an initial rapid distribution half-life (T1) and a second slower half-life (T2). T2 was directly related to the size of the aggregates. High molecular weight [125I]AIgA, containing 10-12 IgA molecules per aggregate [( IgA]10-12), was cleared much faster than low molecular weight aggregates. The main site of clearance was the liver. The larger the size of the AIgA, the more degradation products were found in the circulation. After injection of [IgA]10-12, non-parenchymal cells (NPC) contained three times more radioactivity than parenchymal cells (PC) (NPC:PC ratio 3.06 +/- 0.96). Ratios of 0.82 +/- 0.03 and 0.62 +/- 0.12 were observed when [IgA]5-6 and [IgA]2 were injected respectively, suggesting a greater role for Kupffer cells in the clearance of large-sized IgA aggregates. Kupffer cells were shown to be the main cells for localization of large-sized AIgA established by immunohistochemical staining on liver cryostat sections.

Animals↗
PubMed1990

Inflammatory bowel disease and ankylosing spondylitis associated with cutaneous vasculitis, glomerulonephritis, and circulating IgA immune complexes.

Two patients both with inflammatory bowel disease (IBD) and ankylosing spondylitis (AS) developed leucocytoclastic vasculitis of the skin and nephropathy. Immunofluorescence studies showed that there was perivascular deposition of immunoglobulin A in the skin biopsy specimens of both patients and in the renal mesangium of one patient. Serum samples of the two patients contained IgA immune complexes. The absence of previous reports on such a combination of symptoms in IBD or AS suggests that these patients may have a disease entity which is distinct from uncomplicated IBD or AS, and which may combine the immunopathological features of both underlying disorders.

Adolescent↗
PubMed1990

Value of anti-neutrophil cytoplasmic autoantibodies and other laboratory parameters in follow-up of vasculitis.

The presence of anti-neutrophil cytoplasmic autoantibodies (ANCA), detected by indirect immunofluorescence, is of high sensitivity and specificity in the diagnosis of Wegener's granulomatosis and related diseases, associated with vasculitis. Titres of immunofluorescence are thought to closely reflect disease activity. In a retrospective series of 266 sera of 23 patients with at least one positive test for ANCA, disease activity was correlated with ANCA, assayed by immunofluorescence and by enzyme-linked immunosorbent assay; with rheumatoid factor and with erythrocyte sedimentation rate. All tests were of limited value in predicting disease activity or relapse. A normal sedimentation rate and, to a lesser extent, a negative result of ANCA-immunofluorescence, were useful in excluding active disease.

Autoantibodies↗
PubMed1990

Specificity and cross-reactive idiotypes of anti-gp330 autoantibodies in active Heymann nephritis.

The aim of this study was to characterize the epitope specificity and the idiotype(s) of gp330-specific autoantibodies in active Heymann nephritis (HN). To study this, two monoclonal autoantibodies (mAb), 3D9B and 5B8C, derived from Lewis rats with HN, were generated. These antibodies bound to different epitopes on the autoantigen gp330, as shown by in vitro studies. In order to characterize the idiotype(s) of the mAb, rabbit anti-idiotypic antisera were prepared. It was shown that the rabbit antisera directed against the 3D9B as well as the 5B8C idiotype were able to inhibit the binding of nephritic eluate to gp330. This indicated that the idiotypes recognized on 3D9B and 5B8C were relevant to the spectrum of idiotypes involved in HN. In order to investigate the nature of the two idiotypes of these mAb, cross-absorption and binding studies were performed. The rabbit antisera raised against one of the two idiotypes bound in a direct binding ELISA to both idiotypes. Since the observed cross-reactivity of the antisera suggested that the idiotypes of 3D9B and 5B8C were at least partly cross-reactive, homologous polyclonal and monoclonal anti-idiotypic antibodies were prepared by immunizing rats with 3D9B or 5B8C. The results from the binding and inhibition experiments strongly suggest that the idiotypes of 3D9B and 5B8C contain cross-reactive or public idiotopes.

Animals↗
PubMed1990

IgD immune complex vasculitis in a patient with hyperimmunoglobulinemia D and periodic fever.

We describe a 27-year-old Dutch woman with the hyperimmunoglobulinemia D and periodic fever syndrome. During febrile attacks she occasionally presented with skin lesions on the distal parts of her upper and lower extremities, with the histologic picture of a leukocytoclastic vasculitis. Clear perivascular deposits of IgD and C3 were presented in early lesional skin on immunofluorescence investigation. Circulating IgD immune complexes were demonstrated on several occasions, both during and in between clinical attacks. These findings are consistent with an IgD immune complex-mediated pathogenesis for the skin lesions. In 10 patients with other forms of immune complex vasculitis of the skin, minimal perivascular deposits of IgD were found in four cases. In these cases, however, IgD was never found as the solitary immunoglobulin class.

Adult↗
PubMed1990

[The pathogenesis of primary IgA-nephropathy].

The pathogenesis of IgA nephropathy has remained elusive in the twenty years that have passed since the first description of the disease. Based on the recent literature, we present a pathogenetic model in which a primary disorder of immune regulation plays a central role. This disorder of immune regulation results in an increased synthesis of plasma IgAI antibodies by the bone marrow, in response to everyday mucosal infections. Through an unknown mechanism, these circulating IgAI antibodies deposit in the mesangium, and cause an inflammatory response.

Antibodies, Anti-Idiotypic↗