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Biomedical subjects

M Dueymes

Publications and source records attributed to M Dueymes.

45 records · Page 3Linked to original sources
PubMed1986

Prevention of lupus diseases in MRL/1, NZBxNZW, and BXSB mice treated with a cyclophosphazene derived drug.

A polyclonal activation of lymphocytes (PA) has been suggested to play a pathogenic role in autoimmune and immune complex diseases, particularly in mouse lupus. "DIAM 4," a cyclophosphazene derived drug, selected on the basis of its ability to modulate a PA has been used to treat female MRL/1, female NZBxNZW, and male BXSB mice. In these three strains of mice, the treatment was found to induce an inhibition of the PA, to prevent the increase of anti-DNA antibody levels and the simultaneous decrease of C3 levels, to prevent the appearance of proteinuria, the deposition of immune complexes in glomeruli, and the development of kidney lesions. Moreover in MRL/1 mice, lymphoproliferation was prevented. These results suggest that drugs able to modulate a PA might be efficient in the treatment of mouse lupus nephritis. Such a principle of immunomodulation might open the way to new possibilities of treatment of lupus and other immune complex diseases.

Albuminuria↗
PubMed1986

Polyclonal activation of lymphocytes induced in the mouse by acebutolol, a beta blocking agent.

Acebutolol, a beta blocking agent, was injected at a dose of 1 mg/day, every day for 6 months in C57B1/6 and OF1 mice. No antinuclear antibodies were induced but a transient induction of anti-single stranded DNA antibodies and an increase of IgM, IgA and IgG2a levels were observed during the first 3 weeks in some treated mice as compared to control mice. This effect was more pronounced in C57B1/6 than in OF1 mice and in the C57B1/6 mice, was more frequently observed in female than in male mice. It was further found by cellular studies done in C57B1/6 female mice, that daily i.p. or oral administration of Acebutolol induces a transient polyclonal stimulation of lymphocytes. It is concluded that certain beta blockers might possess some in vivo effects on the immune system.

Acebutolol↗
PubMed1985

In vivo modulation of polyclonal activation of lymphocytes by SOAz, a cyclophosphazene derived drug. Prevention of murine glomerulonephritis induced by chronic injections of lipopolysaccharide.

The effects of a cyclophosphazene derived drug (SOAz), on the polyclonal activation of B lymphocytes induced by bacterial lipopolysaccharide (LPS) have been studied in C57B1/6 mice. It has been found that this drug is able to inhibit the polyclonal stimulation of lymphocytes and a dose-dependent effect has been observed. The therapeutic effects of SOAz injected five times a week at 40 mg/kg/day have been investigated in mice chronically injected with LPS (twice a week, 2.5 mg/kg/day) which developed an immune complex type of glomerulonephritis. A marked prevention of glomerular lesions and of deposits of IgM and IgG, and of the third complement component has been found in mice treated with SOAz as compared to not treated mice.

Animals↗
PubMedDate not supplied

Comparison of cell-ELISA, flow cytometry and Western blotting for the detection of antiendothelial cell antibodies.

OBJECTIVE: There is still great uncertainty in the detection of antiendothelial cell antibodies (AECA). The aim of our study was to compare the results obtained using different methods. METHODS: Sera were obtained from 71 patients with a variety of vasculitides. Three assay methods were used: cell ELISA, flow cytometry (FACS) and Western blot (WB). RESULTS: In the ELISA 12/17 patients with systemic lupus erythematosus (SLE), 1/12 with Churg Strauss (CS) disease, 3/12 with micropolyarteritis (MPA) and 5/30 with Wegener's granulomatosis (WG) tested positive. Most of the sera that were positive on ELISA were not by FACS. Among the negative sera, 50% of WG, 40% of MPA, 20% of CS and 40% of SLE became positive on WB. There were some specific patterns of reactivity for a given disease, so that some bands could be assigned to a disease. CONCLUSION: The discrepancies in the results may most probably be accounted for by differences between the antigenic preparations. Caution must thus be exercised when interpreting the results of any of these three tests.

Arteritis↗
PubMedDate not supplied

Anti-endothelial cell reactivity, the unresolved enigma.

Not only are some anti-endothelial cell antibodies (AECA) directed to thus far unidentified cell membrane structures, but some ot them recognize "planted" antigens and possibly ligand-receptor complexes. The functional heterogeneity of AECA is widely acknowledged: part of them activate the complement, mediate antibody-dependent cell cytotoxicity of trigger the production of tissue procoagulant factor. It has also recently been established that a proportion of AECA have the capacity to induce apoptosis of their target cells. In fact, the most direct demonstration of the pathogenicity of AECA is the autoantibody-induced murine model of vasculitis.

Journal Article↗
PubMedDate not supplied

IgA glycosylation abnormalities in the serum of patients with primary Sjögren's syndrome.

Since there is no information regarding the glycosylation status of immunoglobulin A (IgA) in patients with primary Sjögren's syndrome (pSS), the sialic acid and galactose contents of IgA1 and IgA2 were evaluated in 17 pSS patients and in 14 normal controls (NC), using new enzyme-linked immunosorbent assays. The proportion of sialylated IgA1 and IgA2 was augmented (p < 0.001 and < 0.05, compared with NC), whereas that of galactosylated IgA1 and IgA2 was reduced (p < 0.01 and < 0.02, respectively). The level of SA IgA1 correlated the amount of IgA-containing immune complexes (p < 0.01), serum IgA (p < 0.01) and IgA-rheumatoid factor (p < 0.01). This demonstrates a number of IgA abnormalities in pSS patients. There were no correlations between SA and Gal, however, nor could any difference be ascribed to extraglandular manifestations.

Adult↗
PubMedDate not supplied

IgA in Sjögren's syndrome.

Patients with Sjögren's syndrome (SS) display two sets of immunological abnormalities. B cells are oligoclonally activated, resulting in hypergammaglobulinaemia, elevated levels of circulating immune complexes (CIC) and non-organ specific autoantibodies. The cellular arm of the immune response is also involved, as shown by the predominance of activated T cells within the exocrine gland infiltrate. IgA could well bridge the gap between activated B cells and defective T cells and by doing so, play a pivotal role in the pathogenesis of SS. This interpretation is supported by the high proportion of IgA in immunoglobulin(Igl) production at the mucosal level. Additionally, IgA is the Igl class most dependent on T cell help. A number of studies over the past 15 years have reported high levels of serum and secretory IgA, IgA-rheumatoid factor and IgA-containing CIC. A correlation between disease activity and the latter abnormalities has recently been shown. There is, however, a need for longitudinal assessment of total IgA and IgA autoantibodies in order to further evaluate their role in the pathogenesis of the disease.

Antigen-Antibody Complex↗
PubMedDate not supplied

Autoimmune diseases and monoclonal gammopathies.

Rheumatoid arthritis, systemic lupus erythematosus and primary Sjögren's syndrome are nonorgan-specific autoimmune diseases in which serum monoclonal immunoglobulins (MIg) have been identified repeatedly. Conversely, autoimmune traits have been detected in a number of patients with lymphoproliferative disorders such as multiple myeloma, Waldenström's macroglobulinemia and chronic lymphocytic leukemia. The latter cells have even shown to produce multispecific autoantibodies. One connection between connective tissue diseases and Iymphoid malignancies might be established by a limitedfraction of B Iymphocytes expressing the CD5 marker.

Autoimmune Diseases↗