Biomedical subjects

J E Burton-Kee

Publications and source records attributed to J E Burton-Kee.

4 recordsLinked to original sources

PubMed1981

Different cross-reacting circulating immune complexes in Behçet's syndrome and recurrent oral ulcers.

Circulating immune complexes were isolated by 2% polyethylene glycol precipitation from the sera of 15 out of 37 patients with Behçet's syndrome and 11 out of 23 patients with recurrent oral ulcers. The antigenic cross-reactions of the polyethylene glycol precipitates were studied by coating a plastic tube with one complex and adding another 125I-labeled complex in dissociating (acid) conditions. On neutralization, partial reassembly occurred with the complex coating the tube wall, thus indicating cross-reaction with it. In the first 30 complexes studied, the cross-reactions obtained were sorted by computer program into two mutually exclusive subsets of reactions. Two similar homologous subsets of reactions were found in the second group of 29 patients: in total, nine out of 16 ocular, four out of six herpetiform circulating immune complexes in one subset, and four out of seven neurological in the other. A wider pattern of reaction could be detected in addition, which induced most of the Behçet's syndrome and recurrent oral ulcers. Immune complexes from control sera did not cross-react. An exogenous agent could account for the circulating immune complexes' cross-reactions for the group as a whole, and two antigenic determinants of that agent or antigens from different damaged tissues explain the subsets.

Antigen-Antibody Complex↗

PubMed1980

Defective yeast opsonisation of serum in sarcoidosis.

We have studied the opsonising ability of the sera of 49 patients with sarcoidosis. The serum of 11 (22%) patients was defective in this ability, whereas only two (4%) of 46 clinic control subjects and three (7%) of 43 laboratory control subjects showed this defect. The difference between the prevalence of the defect in sarcoidosis and the control groups was statistically significant (p less than 0.01). Although the patients with sarcoidosis who had this defect tended to have pulmonary infiltration, this relationship was not statistically significant. Similarly, there was no correlation between the activity of sarcoidosis and this defect, although there was a significant (p less than 0.05) relationship between the opsonising defect and the persistence of circulating immune complexes. Serum opsonisation is a genetically linked host defense mechanism. Our findings suggest that the presence of this serum defect may render a person more susceptible to sarcoidosis.

Adolescent↗

PubMed1980

Circulating immune complexes in sarcoidosis.

The sera of 50 patients with sarcoidosis were tested for the presence of circulating immune complexes using polyethylene glycol precipitation, followed by single radial immuno diffusion for the amounts of Clg, IgG, IgM, and double diffusion for the presence of IgA. Complexes were detected in 29 (58%) patients. No correlation could be found between the presence of these complexes and the length of history stage, or activity of disease, nor to steroid therapy. Rheumatoid factor was detected in 14 patients (28%), 13 of whom had circulating immune complexes, and 12 of whom had active disease. Total serum C3, CH50, and Clq were normal, as were immunoglobulin levels. In patients with extrathoracic sarcoidosis, especially skin or joint involvement, complexes were commonly found. The aetiological significance of these complexes remains uncertain.

Adolescent↗

PubMed1980

Defective yeast opsonisation of serum in tuberculosis.

We have studied the opsonising ability of the sera of 92 patients with tuberculosis. Fourteen per cent of these patients showed defective opsonising ability compared with 4% in a clinic control group. This increased frequency in TB was accounted for by the greatly increased proportion with defects found in patients with intrathoracic TB (21%). We may have identified a section of the population with a specific genetically linked abnormality of a host defence mechanism which renders them more susceptible to intrathoracic TB. Further population studies are required.

Adolescent↗