BACKGROUND: Telomeric hexamer repeats (TTAGGG/CCCTAA)n are highly repetitive sequences of DNA. They cap the termini of eukaryotic chromosomes and stabilize them, preventing degradation or fusion. Anti ds-DNA is one of the most specific tests for systemic lupus erythematosus (SLE). Of related importance, a preliminary report has suggested that anti-telomere antibodies are also highly specific for the presence of SLE. METHODS: 220 patients with SLE, 79 with rheumatoid arthritis (RA), 54 with other rheumatic diseases and 99 healthy controls were tested for anti-telomere antibody as measured by enzyme immunoassay detecting 30- and 60-mer telomeric repeats (5-10 hexamers). 48 of the 220 SLE patients charts were abstracted for 90 separate clinical, laboratory and treatment parameters. Comparisons were made between SLE and non-SLE patients, and within the lupus group for telomere positivity and among the latter 48 patients for anti-DNA (Farr) levels and SLEDAI scores. RESULTS: Anti-telomere antibody was present in 48.6% of the overall SLE group (220), 71% of our cohort (48), 11% with primary Sjogren's (2/18), 7. 6% with RA (6/79) and 2% of normal controls (2/99) (P<0.001 comparing SLE to all other groups). In the 48 patient cohort, anti-telomere antibody was more sensitive than anti-dsDNA (Farr) (71% vs 50%), but did not correlate with other clinical parameters, SLEDAI scores, or other autoantibodies. CONCLUSIONS: The detection of anti-telomere antibody appears to be more sensitive and may be as specific as anti-dsDNA (Farr) in SLE. The detection of telomeric repeats may be as accurate as other anti-DNA assay methodologies and more specific for the presence of SLE. The immunogenic potential of telomere biology related to the pathogenesis and/or diagnosis of SLE deserves further investigation.
BACKGROUND: Telomeric hexamer repeats (TTAGGG/CCCTAA)n are highly repetitive sequences of DNA. They cap the termini of eukaryotic chromosomes and stabilize them, preventing degradation or fusion. Anti ds-DNA is one of the most specific tests for systemic lupus erythematosus (SLE). Of related importance, a preliminary report has suggested that anti-telomere antibodies are also highly specific for the presence of SLE. METHODS: 220 patients with SLE, 79 with rheumatoid arthritis (RA), 54 with other rheumatic diseases and 99 healthy controls were tested for anti-telomere antibody as measured by enzyme immunoassay detecting 30- and 60-mer telomeric repeats (5-10 hexamers). 48 of the 220 SLEpatients charts were abstracted for 90 separate clinical, laboratory and treatment parameters. Comparisons were made between SLE and non-SLEpatients, and within the lupus group for telomere positivity and among the latter 48 patients for anti-DNA (Farr) levels and SLEDAI scores. RESULTS: Anti-telomere antibody was present in 48.6% of the overall SLE group (220), 71% of our cohort (48), 11% with primary Sjogren's (2/18), 7. 6% with RA (6/79) and 2% of normal controls (2/99) (P<0.001 comparing SLE to all other groups). In the 48 patient cohort, anti-telomere antibody was more sensitive than anti-dsDNA (Farr) (71% vs 50%), but did not correlate with other clinical parameters, SLEDAI scores, or other autoantibodies. CONCLUSIONS: The detection of anti-telomere antibody appears to be more sensitive and may be as specific as anti-dsDNA (Farr) in SLE. The detection of telomeric repeats may be as accurate as other anti-DNA assay methodologies and more specific for the presence of SLE. The immunogenic potential of telomere biology related to the pathogenesis and/or diagnosis of SLE deserves further investigation.