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CR1 density polymorphism and expression on erythrocytes of patients with systemic lupus erythematosus
13rd Department of Medicine, University Medical School of Debrecen, Hungary.
Insights
Systemic lupus erythematosus (SLE) patients show reduced complement receptor 1 (CR1) on erythrocytes, especially those with kidney involvement. This deficiency appears acquired, not solely genetic.
Area of Science:
- Immunology
- Genetics
- Nephrology
Background:
- Complement Receptor 1 (CR1) plays a role in immune regulation.
- Reduced CR1 expression on erythrocytes has been observed in systemic lupus erythematosus (SLE).
Purpose of the Study:
- To investigate the relationship between CR1 expression on erythrocytes and CR1 density genotype in SLE patients.
- To determine if decreased CR1 expression correlates with disease severity, specifically kidney involvement.
Main Methods:
- Genotyping of CR1 density using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).
- Quantification of CR1 binding sites on erythrocytes using monoclonal anti-CR1.
- Comparison between 46 SLE patients and 47 healthy volunteers.
Main Results:
- SLE patients exhibited fewer CR1 binding sites on erythrocytes compared to healthy individuals with similar CR1 genotypes.
- A significant correlation was found between decreased CR1 expression and kidney involvement in SLE patients homozygous for the high-density CR1 allele (HH).
Conclusions:
- The reduced expression of CR1 on erythrocytes in this SLE cohort is likely an acquired deficiency.
- CR1 erythrocyte expression may serve as a biomarker for kidney involvement in SLE patients with specific genotypes.
Abstract:
The present study investigated the expressed number of CR1 on erythrocytes (E) in relationship of the CR1 density genotype from 46 patients with systemic lupus erythematosus (SLE) and 47 healthy volunteers. The CR1 genotype was determined by a method based on polymerase chain reaction (PCR) amplification of the genomic DNA fragment of 1.8 kb separated by HindIII endonuclease digestion and agarose gel electrophoresis. Our data supported the earlier results that the number of binding sites/E for monoclonal anti-CR1 decreased among SLE patients compared with normal individuals having the same alleles for the CR1/E density. At the same time the novelty of our recent results was that the decreased expression of CR1 on E correlated significantly with kidney involvement in patients homozygous for the CR1/E high density allele (HH). These data suggest that the deficiency of the detectable number of CR1 on erythrocytes is acquired in this SLE population.