OBJECTIVE: To compare autoantibody responses to the collagen-like region of Clq (ClqCLR) with responses to double stranded DNA (dsDNA) and native rat collagen type II during changes of disease activity in patients with systemic lupus erythematosus (SLE). METHODS: IgG antibodies to ClqCLR, dsDNA, and collagen type II were determined by ELISA in serial samples from 33 patients with SLE with different disease manifestations. Antibodies to dsDNA were also detected with the Crithidia luciliae test. RESULTS: Distinct antibody responses in conjunction with flare were observed, but the markers were more clearly related to clinical groups and to severity of disease than to changes of disease activity. Anti-ClqCLR antibodies were detected in 2/10 patients with mild flares, 7/12 patients with severe extrarenal flares, and in 10/11 of the patients with active lupus glomerulonephritis. Findings with regard to anti-dsDNA antibodies were similar. Antibody responses to collagen type II were detected in 7/12 of the patients with severe extrarenal disease, and were less frequently found in the other patients. ELISA absorption and elution experiments with anti-ClqCLR antibodies in the patient sera did not suggest cross reactivity with collagen type II and dsDNA. CONCLUSION: Serial investigation of 33 patients with SLE showed that antibodies to ClqCLR and dsDNA are markers of severe SLE, particularly SLE with kidney involvement. Antibodies to collagen type II are possible markers of severe extrarenal SLE with vasculitis and serositis. Analysis of anti-ClqCLR antibodies provided no evidence of cross reactivity with collagen type II and dsDNA.
OBJECTIVE: To compare autoantibody responses to the collagen-like region of Clq (ClqCLR) with responses to double stranded DNA (dsDNA) and native rat collagen type II during changes of disease activity in patients with systemic lupus erythematosus (SLE). METHODS: IgG antibodies to ClqCLR, dsDNA, and collagen type II were determined by ELISA in serial samples from 33 patients with SLE with different disease manifestations. Antibodies to dsDNA were also detected with the Crithidia luciliae test. RESULTS: Distinct antibody responses in conjunction with flare were observed, but the markers were more clearly related to clinical groups and to severity of disease than to changes of disease activity. Anti-ClqCLR antibodies were detected in 2/10 patients with mild flares, 7/12 patients with severe extrarenal flares, and in 10/11 of the patients with active lupus glomerulonephritis. Findings with regard to anti-dsDNA antibodies were similar. Antibody responses to collagen type II were detected in 7/12 of the patients with severe extrarenal disease, and were less frequently found in the other patients. ELISA absorption and elution experiments with anti-ClqCLR antibodies in the patient sera did not suggest cross reactivity with collagen type II and dsDNA. CONCLUSION: Serial investigation of 33 patients with SLE showed that antibodies to ClqCLR and dsDNA are markers of severe SLE, particularly SLE with kidney involvement. Antibodies to collagen type II are possible markers of severe extrarenal SLE with vasculitis and serositis. Analysis of anti-ClqCLR antibodies provided no evidence of cross reactivity with collagen type II and dsDNA.
Authors: José Pardos-Gea; Josefina Cortés-Hernández; Jesus Castro-Marrero; Eva Balada; José Ordi-Ros Journal: Clin Rheumatol Date: 2017-03-10 Impact factor: 2.980
Authors: Anders Carlsson; Dirk M Wuttge; Johan Ingvarsson; Anders A Bengtsson; Gunnar Sturfelt; Carl A K Borrebaeck; Christer Wingren Journal: Mol Cell Proteomics Date: 2011-02-24 Impact factor: 5.911