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Biomedical subjects

H Moutsopoulos

Publications and source records attributed to H Moutsopoulos.

11 recordsLinked to original sources
PubMed1990

Association of DR4 related RFLP bands and RA in Greeks.

Using the Taq1 restriction enzyme and DR beta, DQ alpha probes, the DNAs of Greek RA patients and controls were characterised for RFLP's associated with DR4. Three DR beta bands, 14.8kb, 6.1kb and 5.4kb were observed at significantly higher frequency in the patients compared with controls. By using a DQ alpha probe, the 2.6kb band (associated with DR1, DRw10, DRBR and DRw14 (Dw9)) was at a significantly raised frequency in the patients. The DQ alpha 5.3kb band associated with DR4, DR7 and DR9 was also raised in the RA patients although this increase did not reach statistical significance. In view of the previously documented lack of association between DR4 (and other DR antigens) and RA in Greeks, the results suggest that some degree of HLA class II association exists with RA in this population at the DNA level which may not be overtly reflected serologically.

Adult↗
PubMed1977

Immune complexes in hepatitis B antigen-associated periarteritis nodosa. Detection by antibody-dependent cell-mediated cytotoxicity and the Raji cell assay.

A subpopulation of peripheral blood lymphocytes with the ability to lyse target cells coated with specific antibody (antibody-dependent cell-mediated cytotoxicity, ADCC) was serially studied in a patient with hepatitis B antigen-associated periarteritis nodosa. The effector lymphocytes possess FC and complement receptors but do not require complement for functional activity. We found that the patient's ADCC was decreased during periods of disease activity and was almost normal during remission. The patient's serum could block ADCC in normal lymphocytes, and the blocking ability correlated with the concentration of immune complexes as determined by the Raji cell assay (a radioimmunoassay using complement receptors on human cultured lymphoblastoid cells). The concentration of immune complexes and the ADCC blocking ability of ther serum both correlated with disease activity. Serum from five other patients with active vasculitis was found to contain significant amounts of immune complexes and was able to block normal ADCC. It appears that the ADCC assay can be used to detect the presence of circulating immune complexes and to monitor disease activity in periarteritis nodosa.

Adult↗
PubMed1976

Antibody-dependent cell-mediated cytotoxicity in selected autoimmune diseases.

Antibody-dependent cell-mediated cytotoxicity mediated by peripheral blood lymphocytes was studied in patients with systemic lupus erythematosus, polyarteritis nodosa. Sjogren's syndrome, and rheumatoid arthritis. The target cells were chicken erythrocytes coated with rabbit anti-chicken erythrocyte antibody. Antibody-dependent cell-mediated cytotoxic activity was normal in Sjogren's syndrome and rheumatoid arthritis but significantly decreased (P is less than 0.001) in active systemic lupus erythematosus and in two patients with polyarteritis nodosa. A partial regeneration of antibody-dependent cell-mediated cytotoxic activity was obtained by treatment with pronase and DNase followed by overnight incubation. Sera from patients with systemic lupus erythematosus inhibited antibody-dependent cell-mediated cytotoxic activity of normal lymphocytes. The inhibitory activity was studied by specific immunoadsorption and sucrose density geadient ultracentrifugation. Removal of IgG but not IgM greatly reduced inhibition. Inhibitory factors were present in 7S and heavier fractions containing IgG. Five systemic lupus erythematosus patients were studied serially to determine if improvement in clinical status could be correlated with a decrease in serum inhibitory factors as studied by inhibition of normal antibody-dependent cell-mediated cytotoxicity. Indeed, a greater serum inhibitory capacity was found in each patient during periods of greater disease activity.

Adult↗
PubMed1976

In vitro effect of thymosin on T-lymphocyte rosette formation in rheumatic diseases.

The in vitro effect of calf thymosin fraction 5 on T-rosette forming cells (E-RFC) was studied in Sjögren's syndrome (SS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). The baseline percent E-RFC in sixteen normal controls was67-2 +/- 6-9. E-RFC was significantly decreased in SLE (42-6 +/- 17-0, P less than 0-0001) and SS (51-8 +/- 16-9, P less than 0-002) but not in RA (59-7 +/- 14-1). Ten of twenty-five SS patients and two of eleven RA patients had less than 50% E-RFC, and all showed a significant increase after incubation with thymosin (+ 16-5 +/- 6-5%, P less than 0-0001, and + 11 +/- 4-9%, P less than 0-001, respectively). Eleven of sixteen SLE patients had less than 50% E-RFC. Their response to thymosin was less dramatic but still statistically significant (+ 5-3 +/- 6-0%, P = 0-03). There was no response to thymosin in control subjects or in patients with baseline E-RFC greater than 50%. No increase in E-RFC was seen after incubation with calf spleen fraction 5 or known stimulators of cyclic-AMP. Sera from four active SLE patients, as well as the supernatant obtained from overnight culture of the lymphocytes from one SLE patients, were able to block T-rosette formation by normal lymphocytes, even after exposure to thymosin. Two 'blocking' sera were fractionated by sucrose density gradient ultracentrifucation. In one, the blocking capacity was found to reside in the 19S region containing IgM. In the second, the blocking capacity was in the 7S region containing IgG. Four 'blocking' lupus sera were depleted of IgG or IgM by immunoabsorption with goat anti-human IgG or goat anti-human IgM sepharose 4B. The blocking ability in three sera was partially decreased by depletion of either IgG or IgM, and in a fourth, only by removing IgG. The percent of lymphocytes staining with fluorescein labelled goat anti-human immunoglobulin antisera was increased in SLE patients (35-9 +/- 20-2 vs 21-7 +/- 5-9 in controls, P = 0-02). After overnight culture, the percent of staining cells decreased to normal values. These results suggest that thymosin can stimulate the differentiation of T-lymphocytes in patients with SS, SLE, and RA when the baseline E-RFC is decreased. Furthermore, the decreased percent E-RFC in SLE is probably due to cell-bound anti-lymphocyte antibodies that block sheep erythrocyte receptors on the T-cell and, possibly, thymosin receptors on undifferentiated lymphocytes.

Adolescent↗
PubMed1976

Low-dosage heparin in rapidly progressive glomerulonephritis.

Two patients developed acute renal failure; creatinine clearances fell to 13 and 34 ml/min, respectively, and one patient was oliguric. Renal biopsies in both patients gave results that were compatible with rapidly progressive glomerulonephritis (RPGN). Both patients were treated with low-dosage heparin sodium infusion (8,000 units/day) and prednisone for two to four weeks, followed by oral anticoagulant (warfarin) and antithrombotic agents (dipyridamole). In the two patients, creatinine clearance rose to at least 60 ml/min, and no bleeding complications were observed. Repeat renal biopsy specimens that were obtained after three to six months of treatment showed no evidence of active glomerulonephritis in either patient, but there was extensive scarring and fibrosis. Low-dosage heparin infusion may arrest and partially reverse the renal failure associated with RPGN in some cases, while avoiding the bleeding complications that are frequently observed in patients treated with larger dosages of heparin.

Administration, Oral↗
PubMedDate not supplied

Association of Sjögren's syndrome with HLA-B8.

HLA antigens were examined by microdroplet lymphocyte cytotoxicity in 31 patients with Sjögrens syndrome. Fifty percent of 22 Causcasian patients (7 of 17 females and 4 of 5 males) had HLA-B8, as compared to 21% of 1205 controls (P=0.002). The presence of HLA-B8 was not correlated with parotid salivary flow, keratoconjunctivitis sicca, or focus score. Because of its association with a number of autoimmune diseases, including Sjögren's syndrome, it is suggested that HLA-B8 is genetically liked to an immune response gene(s) that predisposes the individual to autoimmune phenomena. The expression of autoimmunity may be determined by infectious or environmental factors.

Adolescent↗