The lupus erythematosus cell phenomenon: comparative analysis of antichromatin antibody specificity in lupus erythematosus cell-positive and -negative sera.
OBJECTIVE
To compare and investigate antihistone and antichromatin antibody responses as well as clinical variables in patients with systemic lupus erythematosus (SLE) who were either positive (LEC+) or negative (LEC-) for the lupus erythematosus (LE) cell phenomenon.


METHODS
The binding properties of LEC+ and LEC- SLE sera to chromatin-associated nuclear antigens (histones H1, H2A, H2B, H3, H4; complexes of H2A-H2B, [H2A-H2B]-DNA, H1-DNA; total and H1-stripped chromatin; native and denatured DNA) were investigated. In addition, sera from patients with drug-induced lupus (by procainamide, hydralazine, or quinidine), as well as from patients with rheumatoid arthritis and osteoarthritis, were assessed. Enzyme-linked immunosorbent assay was used to detect specific antibody binding.


RESULTS
Mirroring the important role of histone H1 in the formation of LE cells, anti-histone H1 reactivity was 8-fold higher in LEC+ sera than in LEC- sera. In addition, reactivities to most of the other antigens tested, i.e., other histones and histone-DNA complexes as well as chromatin and DNA, were significantly higher in LEC+ sera than in LEC- sera. All but 1 serum sample from the patients with drug-induced lupus were negative for LE cell formation as well as for anti-histone H1 reactivity, but displayed high antibody reactivities to histone-DNA complexes, including chromatin. Sera from patients with rheumatoid arthritis and osteoarthritis did not show significant binding to these antigens. When comparing the clinical features of LEC+ and LEC- SLE patients, severe organ involvement, including nephritis and central nervous system involvement, was common in the LEC+ group, but rare in the LEC- group.


CONCLUSIONS
A positive LE cell phenomenon not only correlated with the presence of high anti-histone H1 antibody levels in SLE, but also indicated serologically and clinically active disease with major organ involvement.
Schett
G
G
Hannelore Hiesberger, General Hospital Vienna, Medical School, Austria.
Rubin
R L
RL
Steiner
G
G
Hiesberger
H
H
Muller
S
S
Smolen
J
J
D000918:Antibody Specificity; D001172:Arthritis, Rheumatoid / Q000276:immunology; D001323:Autoantibodies / Q000097:blood; D002843:Chromatin / Q000276:immunology*; D006657:Histones / Q000276:immunology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000473:pathology*; D008177:Lupus Vulgaris / Q000139:chemically induced; D009504:Neutrophils / Q000276:immunology; D010003:Osteoarthritis / Q000276:immunology
D001323:Autoantibodies; D002843:Chromatin; D006657:Histones