Rheumatology Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; Division of Rheumatology, Department of Medicine, NYU School of Medicine, New York, NY, USA.
Rheumatology Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
J Autoimmun. 2017 Nov;84:29-45. doi: 10.1016/j.jaut.2017.06.004. Epub 2017 Jun 21.
Oxidation-associated malondialdehyde (MDA) modification of proteins can generate immunogenic neo-epitopes that are recognized by autoantibodies. In health, IgM antibodies to MDA-adducts are part of the natural antibody pool, while elevated levels of IgG anti-MDA antibodies are associated with inflammatory and autoimmune conditions. Yet, in human autoimmune disease IgG anti-MDA responses have not been well characterized and their potential contribution to disease pathogenesis is not known. Here, we investigate MDA-modifications and anti-MDA-modified protein autoreactivity in rheumatoid arthritis (RA). While RA is primarily associated with autoreactivity to citrullinated antigens, we also observed increases in serum IgG anti-MDA in RA patients compared to controls. IgG anti-MDA levels significantly correlated with disease activity by DAS28-ESR and serum TNF-alpha, IL-6, and CRP. Mass spectrometry analysis of RA synovial tissue identified MDA-modified proteins and revealed shared peptides between MDA-modified and citrullinated actin and vimentin. Furthermore, anti-MDA autoreactivity among synovial B cells was discovered when investigating recombinant monoclonal antibodies (mAbs) cloned from single B cells, and 3.5% of memory B cells and 2.3% of plasma cells were found to be anti-MDA positive. Several clones were highly specific for MDA-modification with no cross-reactivity to other antigen modifications such as citrullination, carbamylation or 4-HNE-carbonylation. The mAbs recognized MDA-adducts in a variety of proteins including albumin, histone 2B, fibrinogen and vimentin. Interestingly, the most reactive clone, originated from an IgG1-bearing memory B cell, was encoded by near germline variable genes, and showed similarity to previously reported natural IgM. Other anti-MDA clones display somatic hypermutations and lower reactivity. Importantly, these anti-MDA antibodies had significant in vitro functional properties and induced enhanced osteoclastogenesis, while the natural antibody related high-reactivity clone did not. We postulate that these may represent distinctly different facets of anti-MDA autoreactive responses.
蛋白质的氧化相关丙二醛 (MDA) 修饰可以产生被自身抗体识别的免疫原性新表位。在健康状态下,IgM 抗体是 MDA 加合物的天然抗体库的一部分,而 IgG 抗 MDA 抗体水平升高与炎症和自身免疫性疾病有关。然而,在人类自身免疫性疾病中,IgG 抗 MDA 反应尚未得到很好的描述,其对疾病发病机制的潜在贡献尚不清楚。在这里,我们研究了 MDA 修饰和类风湿关节炎 (RA) 中的抗 MDA 修饰蛋白自身反应性。虽然 RA 主要与瓜氨酸化抗原的自身反应性有关,但我们也观察到 RA 患者血清 IgG 抗 MDA 水平与对照组相比升高。IgG 抗 MDA 水平与 DAS28-ESR 和血清 TNF-α、IL-6 和 CRP 显著相关。对 RA 滑膜组织的质谱分析鉴定了 MDA 修饰蛋白,并发现 MDA 修饰蛋白和瓜氨酸化肌动蛋白和波形蛋白之间存在共享肽。此外,当研究从单个 B 细胞克隆的重组单克隆抗体 (mAb) 时,发现了滑膜 B 细胞中的抗 MDA 自身反应性,并且发现 3.5%的记忆 B 细胞和 2.3%的浆细胞呈抗 MDA 阳性。一些克隆对 MDA 修饰具有高度特异性,与其他抗原修饰(如瓜氨酸化、氨甲酰化或 4-HNE 羰基化)无交叉反应性。这些 mAb 识别包括白蛋白、组蛋白 2B、纤维蛋白原和波形蛋白在内的多种蛋白质中的 MDA 加合物。有趣的是,最具反应性的克隆源自 IgG1 携带的记忆 B 细胞,其编码基因接近原始基因,与先前报道的天然 IgM 相似。其他抗 MDA 克隆显示体细胞高频突变和较低的反应性。重要的是,这些抗 MDA 抗体具有显著的体外功能特性,并诱导增强的破骨细胞生成,而天然抗体相关的高反应性克隆则没有。我们推测,这些可能代表 MDA 自身反应性反应的不同方面。