On day 1, the mean values of L-CR1 transcript (8.42 ± 3.53) and L-CR1 protein (4683 ± 1094) in the SLE patients were 6 times and 12 times lower than the normal controls (n = 103).
Recently, reduced leukocytes CR1 gene transcription had been demonstrated in SLE and was suggested as the main cause of decline in leukocyte CR1 (L-CR1).
We studied the level of leukocyte CR1 transcription in 30 patients with active SLE and 30 controls by reverse transcriptase-polymerase chain reaction (RT-PCR) and related the same with the level of CR1 protein expression monitored by Western blotting.
We have used a combination of three informative restriction fragment length polymorphisms (RFLPs) to assess the frequencies of the F (most frequent allele comprised of four long homologous repeats (LHR)), S (five LHR) and F' (three LHR) alleles of the C3b/C4b receptor (CR1, CD35) in a French population of patients with systemic lupus erythematosus (SLE) (n = 63) and healthy controls (n = 158).
The absence of a significant increase in the frequency of a 6.9-kb band (previously shown to be associated with low-level CR1 on erythrocytes) suggests that this genetic marker does not play a major role in determining SLE, either in these families or in SLE patients in general.
Family studies were carried out to look at CR1 expression in 24 hydralazine-induced SLE patients (Hz Reactors), who had been off the drug for at least 1 year and were clinically well at the time of the study.
The stability over time of the CR1 deficiency among patients, the finding of decreased CR1 number among an expanded group of relatives, the altered frequency among patients of CR1 alleles defined by the HindIII RFLP, and the decreased expression of CR1 on E among patients and relatives compared with normal individuals having the same HindIII RFLP indicate a role for genetic factors in CR1 deficiency in SLE.
B cells from 17 patients with SLE exhibited a mean relative fluorescence for CR1 that was 61% of that found in 17 normal individuals (P less than 0.001).
Polymorphism of the human C3b/C4b receptor. Identification of a third allele and analysis of receptor phenotypes in families and patients with systemic lupus erythematosus.