The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Complement receptor (CR1) deficiency in erythrocytes from patients with systemic lupus erythematosus.
Open accessAbstract
This study reports quantitative information on the concentration of complement receptor for C3b and C4b (CR1) on erythrocytes from normal individuals and patients with immune complex disease. The measurements were performed by an immunoradiometric assay using monoclonal antibodies against CR1. The antibody specificity was confirmed by immunoprecipitation of CR1 from extracts of surface-labeled cells, by inhibition of rosette formation between B lymphocytes and the erythrocytes intermediate EAC14oxy23b, and by the characteristic distribution of the antigen among cells of human peripheral blood. The number of CR1 molecules in erythrocytes from 52 normal individuals was estimated as 1,410 +/- 620. No significant differences in CR1 levels were observed when individuals were grouped by sex, age, or blood groups. In patients with SLE and rheumatoid arthritis, the number of CR1 molecules per RBC was significantly lower, i.e., 600 +/- 307 and 903 +/- 417, respectively. CR1 levels were normal in asthmatics undergoing long-term treatment with prednisone. In SLE patients, significant correlations were found between CR1 levels, C4 hemolytic titers, and levels of circulating immune complexes. In two out of four patients with SLE, CR1 levels increased significantly during remission, showing that the deficiency is, at least in part, reversible. The deficiency in CR1 could be genetically controlled or could represent an epiphenomenon caused by the interaction of the receptor with a ligand present in the circulation of patients.
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Cites
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Cited by
Harold, D., Abraham, R., Hollingworth, P., Sims, R., Gerrish, A., Hamshere, M. L., Pahwa, J. S., Moskvina, V., Dowzell, K., Williams, A., et al. (2009) · Nature Genetics · doi:10.1038/ng.440 · Cited by 3,326
Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
the European Alzheimer's Disease Initiative Investigators, Lambert, J.-C., Heath, S., Even, G., Campion, D., Sleegers, K., Hiltunen, M., Combarros, O., Zelenika, D., Bullido, M. J., et al. (2009) · Nature Genetics · doi:10.1038/ng.439 · Cited by 2,234
Late onset Alzheimer’s disease genetics implicates microglial pathways in disease risk
Efthymiou, A. G., & Goate, A. M. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0184-x · Cited by 562
Medof, M. E., Kinoshita, T., & Nussenzweig, V (1984) · The Journal of experimental medicine · doi:10.1084/jem.160.5.1558 · Cited by 561
Self-citationThe Role of Complement and Its Receptor in the Elimination of Immune Complexes
Epstein, F. H., Schifferli, J. A., Ng, Y. C., & Peters, D. K. (1986) · New England Journal of Medicine · doi:10.1056/nejm198608213150805 · Cited by 396
Metadata
- Authors
- Iida, K., Mornaghi, R., & Nussenzweig, V
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1982-05-01
- Volume
- 155
- Issue
- 5
- Pages
- 1427-1438
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2121291030
- Cited by
- 339
- References
- 23
- FWCI
- 16.66
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Iida, K., Mornaghi, R., & Nussenzweig, V. (1982). Complement receptor (CR1) deficiency in erythrocytes from patients with systemic lupus erythematosus. The Journal of experimental medicine. https://doi.org/10.1084/jem.155.5.1427
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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