Distribution of the HindIII restriction fragment length polymorphism among patients with systemic lupus erythematosus with different concentrations of CR1
- PMID: 1685310
- PMCID: PMC1004554
- DOI: 10.1136/ard.50.11.765
Distribution of the HindIII restriction fragment length polymorphism among patients with systemic lupus erythematosus with different concentrations of CR1
Abstract
Sixty six patients with systemic lupus erythematosus (SLE) were genotyped using a HindIII restriction fragment length polymorphism identified by CR1.1 cDNA, then were followed up for an average of 50 months to evaluate the stability of their CR1 activities. The gene frequencies for the two alleles which correlate with the numeric expression of CR1 on the erythrocytes were not significantly different between 66 patients with SLE and 52 normal controls. A discrepancy between homozygosity for a high allele and a negative CR1 activity was found in many patients. These patients, however, had significantly lower concentrations of serum complement than did patients with a positive CR1, and some were in an active state of the disease. Furthermore, there were several patients in whom the CR1 activities changed from negative to positive together with an increase in serum complement. Our results suggest that the decreased expression of CR1 on erythrocytes in patients with SLE is not inherited, rather it is a consequence of the disease processes.
Similar articles
-
Deficiency of the C3b/C4b receptor (CR1) of erythrocytes in systemic lupus erythematosus: analysis of the stability of the defect and of a restriction fragment length polymorphism of the CR1 gene.J Immunol. 1987 Apr 15;138(8):2708-10. J Immunol. 1987. PMID: 2881967
-
CR1 polymorphism in hydralazine-induced systemic lupus erythematosus: DNA restriction fragment length polymorphism.Clin Exp Immunol. 1989 Dec;78(3):354-8. Clin Exp Immunol. 1989. PMID: 2575471 Free PMC article.
-
Genetic analysis of CR1 expression on erythrocytes of patients with systemic lupus erythematosus.Arthritis Rheum. 1989 Apr;32(4):393-7. doi: 10.1002/anr.1780320407. Arthritis Rheum. 1989. PMID: 2565113
-
Inherited deficiency of erythrocyte complement receptor type 1 does not cause susceptibility to systemic lupus erythematosus.Arthritis Rheum. 1987 Sep;30(9):961-6. doi: 10.1002/art.1780300901. Arthritis Rheum. 1987. PMID: 2959289
-
Structure and function of human complement receptors: 1985.Year Immunol. 1986;2:177-86. Year Immunol. 1986. PMID: 2883788 Review. No abstract available.
Cited by
-
Regulation of circulating immune complexes by complement receptor type 1 on erythrocytes in chronic viral liver diseases.Gut. 2002 Oct;51(4):591-6. doi: 10.1136/gut.51.4.591. Gut. 2002. PMID: 12235086 Free PMC article.
-
Polymorphisms of complement receptor 1 and interleukin-10 genes and systemic lupus erythematosus: a meta-analysis.Hum Genet. 2005 Nov;118(2):225-34. doi: 10.1007/s00439-005-0044-6. Epub 2005 Nov 15. Hum Genet. 2005. PMID: 16133175
-
C3b receptor (CR1) genomic polymorphism in rheumatoid arthritis. Low receptor levels on erythrocytes are an acquired phenomenon.Immunol Res. 1994;13(1):61-71. doi: 10.1007/BF02918226. Immunol Res. 1994. PMID: 7897264
References
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical