OBJECTIVE: To compare the autoantigenicity of the recently described N-terminally elongated PM-Scl-75 protein with that of PM-Scl-100 and the originally defined PM-Scl-75 polypeptide, and to determine its value for analyzing sera from patients with the polymyositis (PM)/scleroderma overlap syndrome. METHODS: Serum samples obtained from patients with the PM/scleroderma overlap syndrome and from patients with several other diseases were analyzed for the presence of autoantibodies reactive with recombinant PM-Scl-100 and PM-Scl-75 (both the original and the longer form) proteins, in an enzyme-linked immunosorbent assay (ELISA). RESULTS: Autoantibodies recognizing the longer PM-Scl-75 protein isoform were detected in 28% of the patients with PM/scleroderma. This percentage is slightly higher than that for PM-Scl-100 (25%) and is significantly higher than that for the previously defined PM-Scl-75 protein (11%). In addition, we identified a significant number of patients who had anti-PM-Scl-75 but not anti-PM-Scl-100 antibodies. This finding contrasts with what has been previously reported for the shorter version of the PM-Scl-75 protein. CONCLUSION: Our data indicate that use of the long PM-Scl-75 isoform in addition to PM-Scl-100 in ELISAs significantly increases the number of patients in whom anti-PM-Scl autoantibodies can be detected.
OBJECTIVE: To compare the autoantigenicity of the recently described N-terminally elongated PM-Scl-75 protein with that of PM-Scl-100 and the originally defined PM-Scl-75 polypeptide, and to determine its value for analyzing sera from patients with the polymyositis (PM)/scleroderma overlap syndrome. METHODS: Serum samples obtained from patients with the PM/scleroderma overlap syndrome and from patients with several other diseases were analyzed for the presence of autoantibodies reactive with recombinant PM-Scl-100 and PM-Scl-75 (both the original and the longer form) proteins, in an enzyme-linked immunosorbent assay (ELISA). RESULTS: Autoantibodies recognizing the longer PM-Scl-75 protein isoform were detected in 28% of the patients with PM/scleroderma. This percentage is slightly higher than that for PM-Scl-100 (25%) and is significantly higher than that for the previously defined PM-Scl-75 protein (11%). In addition, we identified a significant number of patients who had anti-PM-Scl-75 but not anti-PM-Scl-100 antibodies. This finding contrasts with what has been previously reported for the shorter version of the PM-Scl-75 protein. CONCLUSION: Our data indicate that use of the long PM-Scl-75 isoform in addition to PM-Scl-100 in ELISAs significantly increases the number of patients in whom anti-PM-Scl autoantibodies can be detected.
Authors: N Hunzelmann; E Genth; T Krieg; M Meurer; I Melchers; P Moinzadeh; C Pfeiffer; G Riemekasten; E Schulze-Lohoff; C Sunderkoetter; U Müller-Ladner Journal: Z Rheumatol Date: 2008-07 Impact factor: 1.372
Authors: Ulrich A Walker; Philip J Clements; Yannick Allanore; Oliver Distler; Chester V Oddis; Dinesh Khanna; Daniel E Furst Journal: Rheumatology (Oxford) Date: 2017-09-01 Impact factor: 7.580