Premium
High Sensitive Detection of Double‐Stranded DNA Autoantibodies by a Modified Crithidia luciliae Immunofluorescence Test
Author(s) -
Conrad Karsten,
Ittenson Annelore,
Reinhold Dirk,
Fischer Richard,
Roggenbuck Dirk,
Büttner Thomas,
Bosselmann HansPeter,
Steinbach Jörg,
Schößler Werner
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04801.x
Subject(s) - autoantibody , antibody , immunofluorescence , medicine , immunology , anti dsdna antibodies , serology , autoimmune disease , anti nuclear antibody , rheumatology , lupus erythematosus , indirect immunofluorescence
Anti‐double‐stranded (ds)DNA antibodies are serological markers of systemic lupus erythematosus (SLE). Of all anti‐dsDNA antibody detection methods, the Crithidia luciliae immunofluorescence test (CLIFT) is thought to have the highest specificity for SLE. However, the clinical application is hampered by the low diagnostic sensitivity. A CLIFT with modified assay buffer (mCLIFT) was developed and compared with conventional CLIFT, using sera from 110 patients with SLE, 89 anti‐dsDNA ELISA‐positive patients with other diseases (non‐SLE group A), 157 non‐SLE patients with undetectable anti‐dsDNA antibodies by ELISA (non‐SLE group B), 77 disease controls (non‐SLE group C), and 50 healthy blood donors. Out of the 110 anti‐dsDNA antibody ELISA‐positive SLE patients, 84 (76.4%) demonstrated a positive kinetoplast staining, using the mCLIFT, compared to only 42.3%, using the conventional CLIFT. The diagnostic specificity of mCLIFT was 100% with healthy blood donors and 98.1% with the non‐SLE group C (anti‐nuclear antibodies negative; no signs or symptoms of an autoimmune disease) included. In the non‐SLE groups A and B with various other autoimmune diseases or symptoms of a possible autoimmune disease, positive mCLIFT results were obtained in 33.7% and 3.2%, respectively. In conclusion, by modification of the assay buffer, a significant increase in sensitivity of the CLIFT could be observed while retaining the high specificity for SLE. Further investigation is required to check whether the CLIFT‐positive non‐SLE patients develop SLE and whether anti‐dsDNA antibodies detected by the mCLIFT represent a pathogenetic and diagnostic subgroup of autoantibodies that may improve the early diagnosis of SLE or SLE‐overlap syndromes.