Atypical neonatal respiratory syncytial virus infection.
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Biomedical subjects
Publications and source records attributed to A Unger.
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Immunoglobulin production from human B-lymphocytes stimulated in vitro with pokeweed mitogen (PWM) was measured after 11 days of cell culture. IgM and IgG levels in culture supernatants were quantified using ELISA techniques. Addition of the prostaglandin cyclooxygenase inhibitor indomethacin (10(-7) M) to cell cultures concurrently with PWM, inhibited both IgM and IgG synthesis by 80-90% in the four individuals studied. Reduction of immunoglobulin production was apparently concentration-related over the range studied (10(-6)-10(-8) M) and was not associated with cytotoxicity. If this action of indomethacin results from inhibition of cyclooxygenase, then prostaglandins or other arachidonic acid products could be involved in the regulation of human B-lymphocyte immunoglobulin production.
The antibody-dependent cell-mediated cytotoxicity technique (ADCC) and an isotopic antiglobulin technique have been compared for their abilities to detect human serum antibodies to Chang liver cell membrane antigens. The optimal conditions were established for the latter technique, which was found to be superior with respect to reproducibility and sensitivity. Also, unlike ADCC, the isotopic antiglobulin technique was unaffected by other factors, such as immune complexes present in pathological sera.
Immune complexes were measured in the sera of 18 patients iwth ankylosing spondylitis and 5 normal control subjects by their ability to inhibit antibody-mediated lymphocyte-induced cytotoxicity. 11 of the spondylitis and none of the control sera contained circulating complexes. Fractionation of sera on Sephadex G-200 showed that complexes were of two molecular sizes, one of intermediate and the other of large molecular weight. The presence of immune complexes did not correlate with activity of disease or the presence of peripheral arthritis although the one patient with polyarthritis had the highest level of complexes detected in this study. The nature of the antigen in these antigen-antibody complexes is of great interest since it may provide evidence of the aetiological agent in the disease.
Material reacting like carcinoembryonic antigen (CEA) in the radioimmunoassay has been extracted from rheumatoid synovial membranes. This CEA activity has been compared to that found in hepatic metastases from colorectal tumours and in normal adult lung. The antigen in the rheumatoid synovium has been shown to be more sensitive to perchloric acid and to isolate with a lower weight than that derived from the tumour and lung. Immunodiffusion studies with anti-CEA indicate that the CEA-like determinants in the rheumatoid synovium have partial identity with tumour CEA and that a significant proportion of them are associated with large molecular weight material. Production of an antiserum to these CEA-like components in the rheumatoid synovium should enable further identification of their relationship to tumour CEA and might allow a better judgement of whether or not they represent the expression of neoantigens in the disease.
Serum from eleven of fifty-four patients with Hodgkin's disease inhibited phytohaemagglutinin (PHA) stimulation of both autologous and homologous lymphocytes. The inhibitory effect resided in the macromolecular fraction of these sera. PHA was shown to bind to serum substances in inhibitory sera and the degree of PHA binding in the macromolecular fraction correlated directly with the extent of inhibition.
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In an earlier study, the mean plasma carcinoembryonic antigen (CEA) level of patients with seropositive rheumatoid arthritis (RA) was found to be significantly higher than that of normal, control subjects. Levels of CEA in patients with seronegative RA and ankylosing spondylitis, however, did not differ from normal. In this study it was shown that the mean CEA level of 16 patients with Sjögren's syndrome was also significantly higher than normal (P equals 0.001), whereas in a group of 23 children with Still's disease the mean level fell within the normal adult range. Despite the apparent association between rheumatoid factor and raised plasma CEA, no correlation was found between titre of rheumatoid factor and CEA levels. Gel filtration studies indicated that the CEA in rheumatoid arthritis was of a similar molecular weight to that found in cancer of the colon and that there was minimal contribution by the known cross-reacting antigen CCEA2. The mean CEA level in rheumatoid synovial fluids was found to be significantly higher than in osteoarthrotic fluids. A preliminary study has also shown that CEA can be extracted from rheumatoid synovial membranes but was not detected in a normal synovium, further indicating that the source of this antigen in RA may be the inflamed synovium.
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