PT  - JOURNAL ARTICLE
AU  - CAROLINA LLANOS
AU  - EDWARD K.L. CHAN
AU  - SONGQING LI
AU  - GRANT X. ABADAL
AU  - PETER IZMIRLY
AU  - CAROLINE BYRNE
AU  - ROBERT M. CLANCY
AU  - JILL P. BUYON
TI  - Antibody Reactivity to α-Enolase in Mothers of Children with Congenital Heart Block
AID  - 10.3899/jrheum.080860
DP  - 2009 Mar 01
TA  - The Journal of Rheumatology
PG  - 565--569
VI  - 36
IP  - 3
4099  - http://www.jrheum.org/content/36/3/565.short
4100  - http://www.jrheum.org/content/36/3/565.full
SO  - J Rheumatol2009 Mar 01; 36
AB  - Objective. To evaluate the frequency of anti-α-enolase antibodies in the sera of mothers whose children have congenital heart block (CHB), given provocative results in which α-enolase, a membrane protein, was recognized by monoclonal antibodies reactive with the peptide p200 of 52 kDa Ro/SSA in a neonatal rat heart library. Methods. An ELISA using a recombinant α-enolase protein was developed. Sera from 100 anti-Ro52+ CHB mothers in the Research Registry for Neonatal Lupus, 50 patients with systemic lupus erythematosus (SLE; 7 anti-Ro52+), and 48 healthy controls were tested for anti-α-enolase reactivity. Results. There were no significant differences in the median values obtained from CHB mothers, patients with SLE, or controls at each of the dilutions tested. Only 7 (7%) at 1:100 dilution and 2 (2%) at 1:1000 dilution of 100 CHB sera were 3 standard deviations above the mean value obtained for controls. Preincubation with recombinant Ro52 did not inhibit anti-α-enolase reactivity. Conclusion. The low frequency of anti-α-enolase antibodies in the sera of CHB mothers and the absence of apparent cross-reactivity with Ro52 suggest that antibodies to Ro52 are not likely to mediate CHB via binding to α-enolase.