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Biomedical subjects

A Zoma

Publications and source records attributed to A Zoma.

24 records · Page 2Linked to original sources
PubMed1986

Inhibition of complement-mediated solubilisation of antigen-antibody complexes by serum factor(s) in patients with various connective tissue diseases.

Control of immune complex formation is important to limit disease resulting from their deposition in tissues. Any inhibition of immune complex solubilisation is thus significant in the pathogenesis of immune complex diseases. More than half of our patients with various rheumatic connective tissue diseases were demonstrated to have serum inhibition of immune complex solubilisation (12/16 rheumatoid arthritis, 22/37 systemic lupus erythematosus, 16/29 primary Sjogren's syndrome, and eight of nine with mixed connective tissue disease). This serum inhibitory activity did not correlate well with serum levels of IgM rheumatoid factor or circulating immune complexes, and its nature remains to be elucidated.

Antibodies, Antinuclear↗
PubMed1986

Decreased C3b receptors (CR1) on erythrocytes from patients with systemic lupus erythematosus.

Using 125I-F(ab')2 anti-CR1 we have measured C3b receptors (CR1) on the erythrocytes of 56 normal individuals 26 patients with systemic lupus erythematosus (SLE) and 24 with rheumatoid arthritis (RA). The mean number of CR1 sites in SLE (1150/cell) but not RA (1460/cell) was significantly lower (P less than 0.01) than normal (2200/cell). Although the cumulative frequency curve for normals showed minor inflections at frequencies of 18% and 64%, these were not sufficiently marked to permit us to conclude that they distinguished subpopulations of different CR1 phenotypes. Measurement of CR1 numbers of two normal families and four families of SLE patients indicated that low CR1 numbers aggregated in families as did high CR1 numbers, a finding which suggests that CR1 numbers are under genetic control. However, certain observations in SLE patients indicated that low CR1 numbers could be an acquired abnormality. These included, (a) absent CR1 phenotype in a patient whose family had moderate and high CR1 numbers, (b) increasing CR1 numbers as SLE patients went into remission, (c) CR1 numbers were lower in patients with active compared with inactive disease and (d) CR1 numbers were different in each of two sets of identical twins (Fig. 4A). Our conclusions are that, (a) genetic factors probably influence CR1 numbers in normal individuals, (b) that our findings were not inconsistent with the two codominant allele models (Wilson et al., 1982), and (c) the low CR1 phenotype of SLE patients may be secondary to the disease process.

Arthritis, Rheumatoid↗
PubMed1983

Complement-mediated inhibition of immune precipitation in patients with immune complex diseases.

The ability of human sera to prevent the precipitation of antigen-antibody complexes has been investigated. The early complement components including C3 are required for optimal prevention of immune precipitation, whereas the later components are not required. The sera of 36 of 75 patients with seropositive rheumatoid arthritis (RA), 14 of 32 with SLE and four of 17 with glomerulonephritis exhibited reduced capacities to prevent immune precipitation. In contrast sera from patients with seronegative RA, ankylosing spondylitis, psoriatic arthritis or degenerative joint disease were normal in this respect. In SLE and GN sera hypocomplementaemia was frequently associated but not always with failure to prevent immune precipitation, whereas only a small proportion of the patients with seropositive RA and reduced capacity to retain complexes in a soluble form were hypocomplementaemic. Thus the failure of sera to prevent the precipitation of antigen-antibody complexes is not always associated with hypocomplementaemia.

Antigen-Antibody Complex↗