Heterogeneity of circulating immune complexes in chronic lung diseases.
dc.contributor.author | Cooper, K M | |
dc.contributor.author | Moore, Michael | |
dc.date.accessioned | 2011-06-16T21:44:28Z | |
dc.date.available | 2011-06-16T21:44:28Z | |
dc.date.issued | 1982-04 | |
dc.identifier.citation | Heterogeneity of circulating immune complexes in chronic lung diseases. 1982, 7 (3):155-61 J Clin Lab Immunol | en |
dc.identifier.issn | 0141-2760 | |
dc.identifier.pmid | 6980284 | |
dc.identifier.uri | http://hdl.handle.net/10541/133538 | |
dc.description.abstract | Circulating immune complex (IC) levels in sera from 58 healthy controls and a total of 212 patients with various chronic lung diseases were measured using 3 assays. Two complement-dependent assays (C1q fluid phase and Raji) and a complement-independent assay (L1210) were employed. The 3 assays generally revealed similar patterns of reactivity when control and pathological groups were compared, with the L1210 assay invariably demonstrating the lowest incidence of positive values in each group. The most significant elevations in IC levels were exhibited in bronchiectasis and bronchogenic carcinoma. However, within these two groups correlations between IC assays performed on individual sera were poor. Significant but weak correlations (p less than 0.01) were only observed for C1q vs Raji in bronchiectasis and C1q vs L1210 in bronchogenic carcinoma. Complement-binding ICs were present to a similar extent in both conditions. However, non-complement binding ICs were found to be more common in bronchiectasis. The relative sensitivity of the tests and the contribution of interfering factors to the disparity between the assays is discussed. However, the interpretation favoured is that the lack of correlation is primarily a reflection of the intrinsic heterogeneity of immune complexes formed under similar and dissimilar pathological conditions. | |
dc.language.iso | en | en |
dc.subject.mesh | Animals | |
dc.subject.mesh | Antigen-Antibody Complex | |
dc.subject.mesh | Antigens, Heterophile | |
dc.subject.mesh | Bronchiectasis | |
dc.subject.mesh | Carcinoma, Bronchogenic | |
dc.subject.mesh | Chronic Disease | |
dc.subject.mesh | Complement Activating Enzymes | |
dc.subject.mesh | Complement C1q | |
dc.subject.mesh | Complement Fixation Tests | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Immunoglobulin G | |
dc.subject.mesh | Leukemia L1210 | |
dc.subject.mesh | Lung Diseases | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Middle Aged | |
dc.subject.mesh | Preservation, Biological | |
dc.subject.mesh | Pulmonary Fibrosis | |
dc.title | Heterogeneity of circulating immune complexes in chronic lung diseases. | en |
dc.type | Article | en |
dc.identifier.journal | Journal of Clinical & Laboratory Immunology | en |
html.description.abstract | Circulating immune complex (IC) levels in sera from 58 healthy controls and a total of 212 patients with various chronic lung diseases were measured using 3 assays. Two complement-dependent assays (C1q fluid phase and Raji) and a complement-independent assay (L1210) were employed. The 3 assays generally revealed similar patterns of reactivity when control and pathological groups were compared, with the L1210 assay invariably demonstrating the lowest incidence of positive values in each group. The most significant elevations in IC levels were exhibited in bronchiectasis and bronchogenic carcinoma. However, within these two groups correlations between IC assays performed on individual sera were poor. Significant but weak correlations (p less than 0.01) were only observed for C1q vs Raji in bronchiectasis and C1q vs L1210 in bronchogenic carcinoma. Complement-binding ICs were present to a similar extent in both conditions. However, non-complement binding ICs were found to be more common in bronchiectasis. The relative sensitivity of the tests and the contribution of interfering factors to the disparity between the assays is discussed. However, the interpretation favoured is that the lack of correlation is primarily a reflection of the intrinsic heterogeneity of immune complexes formed under similar and dissimilar pathological conditions. |