Expression of the major rheumatoid factor cross-reactive idiotype in pediatric patients with systemic lupus erythematosus

Abstract

Rheumatoid factor cross-reactive idiotype (RF-CRI) is expressed in high concentrations in the sera of some patients with rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA). To determine if RF-CRI is specifically expressed in rheumatic disease or if it is secondary to polyclonal B-cell activation, we examined sera of 23 children with SLE, 16 adolescents with infectious mononucleosis (IM), and age-matched pediatric controls for RF-CRI expression. Concentrations of RF-CRI in serum, determined by an inhibition ELISA, were 24 ± 17 μg/ml (mean ± SD) in 25 normal children, 31 ± 17 in 16 young adults with IM, and were significantly increased, 70 ± 80 μg/ml, in the 23 children with SLE ( p < 0.036). Eleven of 23 SLE patients had serum RF-CRI greater than the mean ± 2 SD for normal children. Ten of 23 SLE sera contained IgM rheumatoid factor (RF) activity. One patient with IM had a borderline elevated RF-CRI level, and 5 IM patients had RF in their sera. The serum IgM concentrations in sera were: SLE (192 ± 93 mg/dl) and IM (234 ± 77 mg/dl) sera. These levels were significantly elevated compared to controls (132 ± 44 mg/dl), p < 0.031 for SLE and p < 0.001 for IM, suggesting that polyclonal activation of B cells was present in SLE and IM patient groups. Increased expression of RF-CRI in the SLE patients correlated directly with high titer anti-DNA antibody values ( r = 0.3965, p < 0.05) and RF activity when human IgG ( r = 0.5026, p < 0.05) was used as the RF binding substrate and inversely with serum C3 levels ( r = 0.3925, p < 0.05). RF-CRI expression did not correlate with RF that bound rabbit ( r = 0.3123, p < 0.05). Increased serum RF-CRI expression is not a result of polyclonal B-cell activation. RF-CRI may be selectively up-regulated in patients with SLE.