Identification of antibodies against extracellular matrix proteins in human osteoarthritis

自身抗体 软骨寡聚基质蛋白 同型 抗体 细胞外基质 免疫学 软骨 骨关节炎 医学 类风湿性关节炎 免疫球蛋白G 化学 分子生物学 生物 病理 单克隆抗体 生物化学 替代医学 解剖
作者
Johannes Ruthard,Gabriele Hermes,Ursula Hartmann,Gerhard Sengle,Georg Pongratz,Benedikt Ostendorf,Matthias Schneider,Stefan Höllriegl,Frank Zaucke,Raimund Wagener,Thomas Streichert,Andreas R. Klatt
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier]
卷期号:503 (3): 1273-1277 被引量:16
标识
DOI:10.1016/j.bbrc.2018.07.036
摘要

We investigated the presence of autoantibodies against the extracellular matrix proteins thrombospondin-4 (TSP-4), cartilage oligomeric matrix protein (COMP), C-type lectin domain family 3 member A (CLEC3A), collagen II, collagen VI, matrilin-3, and fibrillin-2 in the serum of osteoarthritis (OA) patients. We compared those results with the presence of such antibodies in rheumatoid arthritis (RA) patients and in healthy donors (HD). Our study examines whether antibodies against extracellular proteins can be used as potential biomarkers to support the clinical diagnosis of OA. 10 OA, 10 RA patients and 10 HD were enrolled in this explorative cross-sectional study. SDS-PAGE and immunoblot were used to investigate the presence of antibodies against extracellular matrix proteins. The serum of 5/10 OA patients but 0/10 HD exhibited TSP-4 IgG isotype antibodies (P = 0.033). The serum of 8/10 OA patients but only 1/10 HD exhibited IgG isotype antibodies against TSP-4 or COMP (P = 0.005). The serum of 9/10 OA patients but only 1/10 HD exhibited IgG isotype antibodies against TSP-4, COMP or CLEC3A (P = 0.005). We found strong evidence for the presence of IgG isotype autoantibodies against the cartilage extracellular matrix proteins TSP-4, COMP and CLEC3A in OA. The detection of IgG isotype autoantibodies against TSP-4, COMP and CLEC3A may support the clinical diagnosis of OA. OA with autoantibodies against cartilage extracellular matrix proteins defines a new OA subgroup suggesting that patients with high concentrations of autoantibodies may benefit from an immune suppressive therapy.

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