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Correction to: The citrullinated/native index of autoantibodies against hnRNP-DL predicts an individual “window of treatment success” in RA patients
Arthritis Research & Therapy ( IF 4.4 ) Pub Date : 2021-10-09 , DOI: 10.1186/s13075-021-02639-z
Bianka Marklein 1 , Madeleine Jenning 1, 2 , Zoltán Konthur 3, 4, 5 , Thomas Häupl 1 , Franziska Welzel 3 , Ute Nonhoff 3 , Sylvia Krobitsch 3 , Debbie M Mulder 6 , Marije I Koenders 6 , Vijay Joshua 7 , Andrew P Cope 8 , Mark J Shlomchik 9 , Hans-Joachim Anders 10 , Gerd R Burmester 1 , Aase Hensvold 7, 11 , Anca I Catrina 7 , Johan Rönnelid 12 , Günter Steiner 13, 14 , Karl Skriner 1, 2
Affiliation  

Correction to: Arthritis Res Ther 23, 239 (2021)

https://doi.org/10.1186/s13075-021-02603-x

Following publication of the original article [1], the authors reported an error in Additional file 1 wherein the track changes are visible. The Additional file 1 has been updated.

The original article [1] has been updated.

  1. 1.

    Marklein B, Jenning M, Konthur Z, et al. The citrullinated/native index of autoantibodies against hnRNP-DL predicts an individual “window of treatment success” in RA patients. Arthritis Res Ther. 2021;23:239. https://doi.org/10.1186/s13075-021-02603-x.

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Affiliations

  1. Department of Rheumatology and Clinical Immunology, Charité — Universitätsmedizin Berlin, Charite Campus Mitte, Rheumatologisches Forschungslabor - AG Skriner, Chariteplatz 1 (intern Virchowweg 11, 5.OG, R011), 10117, Berlin, Germany

    Bianka Marklein, Madeleine Jenning, Thomas Häupl, Gerd R. Burmester & Karl Skriner

  2. German Rheumatism Research Centre, Leibniz Institute, 10117, Berlin, Germany

    Madeleine Jenning & Karl Skriner

  3. Max Planck Institute for Molecular Genetics, Berlin, Germany

    Zoltán Konthur, Franziska Welzel, Ute Nonhoff & Sylvia Krobitsch

  4. Max Planck Institute of Colloids and Interfaces, Potsdam, Germany

    Zoltán Konthur

  5. Department of Analytical Chemistry (Dpt.1), Bundesanstalt für Materialforschung und-prüfung (BAM), Berlin, Germany

    Zoltán Konthur

  6. Department of Experimental Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands

    Debbie M. Mulder & Marije I. Koenders

  7. Division of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden

    Vijay Joshua, Aase Hensvold & Anca I. Catrina

  8. Centre for Rheumatic Diseases, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King’s College London, London, UK

    Andrew P. Cope

  9. Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

    Mark J. Shlomchik

  10. Medical Clinic and Policlinic IV, Nephrological Center, Ludwig-Maximilian-University Hospital, Munich, Germany

    Hans-Joachim Anders

  11. Academic Specialist Center, Center for Rheumatology, Stockholm Health Region, Stockholm, Sweden

    Aase Hensvold

  12. Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden

    Johan Rönnelid

  13. Division of Rheumatology, Medical University of Vienna, Vienna, Austria

    Günter Steiner

  14. Ludwig Boltzmann Cluster for Arthritis and Rehabilitation, Vienna, Austria

    Günter Steiner

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Corresponding author

Correspondence to Karl Skriner.

Additional file 1:

Figure 1. Sequence, structure and major immunogenic region (mir) of hnRNP-D and hnRNP-DL. A, Schematic representation of hnRNP-D (isoform p45), hnRNP-DL and the different recombinant hnRNP-DL variants studied. The main structural features are highlighted. Mir-region is the major immunogenic region, RBD1 and RBD2 are RNA-binding domains 1 and 2, Gly-rich is the C-terminal glycine-rich region of the proteins. B, Global amino acid sequence alignment of hnRNP-D and hnRNP-DL1 (isoform 1). HnRNP-D and -DL share 89.1% similarity by sequenc e[1]. Regions “mir”, “RBD1”, “RBD2” and “Gly-rich” are highlighted. Figure 2. Characterisation of autoantibodies against, A, citrullinated α-hnRNP-DLmir (cit-DL), B, α-hnRNP-DLmir (DL) and C, ΔOD between cit-DL and DL (ΔDL) determed by ELISA in sera of other diseases (n=127; MS n=20, reA n=7, Sclero n=20, Sjö n=20, PsA n=20, MB n=20, OA n=20). The dotted lines markes the cutoff vs. other diseases (except systemic lupus erythematosus) or healthy controls with 98% specificity each. OD, optical density; nm, nano meter; vs., versus; MS, multiple sclerosis; reA, reactive arthritis; Sclero, scleroderma; Sjö, Sjögren´s syndrome; PsA, psoriasis arthritis; MB, ankylosing spondylitis; OA. Osteoarthritis. Table 1. Mann Whitney U-test of (cit) α-hnRNP-DLmir-OD signals of seropositive and seronegative data sets of RA-cohorts. Table 2. Mann Whitney U-test of cit α-hnRNP-DLmir-OD signals of seronegative data sets of RA-cohorts and data sets of other inflammatory diseases. Figure 3. XY-Plot and Spearman Correlation of citrullinated or native α-hnRNP-DLmir versus ΔhnRNP-DLmir for the early RA cohort EIRA (A/D; n=404), the seropositive EIRA sera (B/E; n=202) and the seronegative EIRA sera (C/F; n=202). Table 3. Spearman correlation of the early RA sera of the EIRA cohort (n=404). The results are given as R value (left of slash) with the corresponding p-value (right of slash). Table 4. Spearman correlation of the 242 EIRA sera treated with MTX (α-CCP2 positive n=133, α-CCP2 negative n=109). The results are given as R value (left of slash) with the corresponding p-value (right of slash). Table 5. Spearman correlation of the established RA sera of the Predict cohort (n=94; RF IgM and/or α-CCP2 positive n=64, RF IgM and α-CCP2 negative n=30). The results are given as R value (left of slash) with the corresponding p-value (right of slash). Table 6. ROC analysis of native hnRNP-DLmir of MTX-treated EIRA patients (n=192; seropositive n=93, seronegative n=99). Table 7. Negative CNDL-index of MTX-treated EIRA patients n=192 (Resp. n=161, non-Resp. n=31). Table 8. ROC analysis of native hnRNP-DLmir of Enbrel®-treated Predict patients (n=94; seropositive n=63, seronegative n=31). Figure 4. High baseline titer against α-hnRNP-DLmir (DL) is rather present in 6-month EULAR Responder RA patients who had received MTX or α-TNF inhibitor therapy (Enbrel®). A-C, Citrullinated α-hnRNP-DLmir (citDL) (A), α-hnRNP-DLmir (DL) (B) and Δ OD between citDL and DL (ΔDL) (C) were measured by ELISA in patient sera from the EIRA cohort treated with MTX (n=192) with 161 EULAR Responder and 31 EULAR non-Responder among 6 months. The evaluation was done according to the cutoff versus other diseases. D, α-DL were measured by ELISA in patient sera from the Predict cohort treated with α-TNF inhibitor therapy with 6-month EULAR response data (n=94, responder n=63, non-Responder n=31). Based on the signals, a response-cutoff (dotted line, OD 0.174) was determined, from which only responders are recognized as positive. OD, optical density; nm, nano meter; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; MTX, Methotrexate; Resp., 6-month EULAR Responder. Figure 5. A, Influence of cytokines on hnRNP-DL expression determined by immunoblotting. Cellular extracts from unstimulated, IL1α- or TNFα-stimulated HeLa cells and from unstimulated and IL6-stimulated HepG2 cells were probed with α-hnRNP-DL1/2-peptide specific rabbit serum. B, Citrullination of hnRNP-DL in synovial tissue from a patient with rheumatoid arthritis was investigated with an α-deiminated arginine antibody and an α-hnRNP-DL antibody. Both positive bands were labled with hnRNP-DL, which isoforms were not analysed.

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Marklein, B., Jenning, M., Konthur, Z. et al. Correction to: The citrullinated/native index of autoantibodies against hnRNP-DL predicts an individual “window of treatment success” in RA patients. Arthritis Res Ther 23, 255 (2021). https://doi.org/10.1186/s13075-021-02639-z

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中文翻译：
更正：针对 hnRNP-DL 的自身抗体的瓜氨酸化/天然指数预测 RA 患者的个体“治疗成功窗口”

更正：关节炎水疗 23, 239 (2021)

https://doi.org/10.1186/s13075-021-02603-x

在原始文章 [1] 发表后，作者在附加文件 1 中报告了一个错误，其中可以看到轨道更改。附加文件 1 已更新。

原文[1]已更新。

  1. 1.

    Marklein B、Jenning M、Konthur Z 等。针对 hnRNP-DL 的自身抗体的瓜氨酸化/天然指数预测了 RA 患者的个体“治疗成功窗口”。关节炎水疗。2021；23:239。https://doi.org/10.1186/s13075-021-02603-x。

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隶属关系

  1. 风湿病学和临床免疫学系，Charité — Universitätsmedizin Berlin, Charite Campus Mitte, Rheumatologisches Forschungslabor - AG Skriner, Chariteplatz 1 (intern Virchowweg 11, 5.OG, R011), 10117, Berlin, Germany

    比安卡·马克林、玛德琳·詹宁、托马斯·豪普、格尔德·R·伯梅斯特和卡尔·斯克林纳

  2. 德国风湿病研究中心，莱布尼茨研究所，10117，柏林，德国

    玛德琳·詹宁和卡尔·斯克林纳

  3. 马克斯普朗克分子遗传学研究所，柏林，德国

    Zoltán Konthur、Franziska Welzel、Ute Nonhoff 和 Sylvia Krobitsch

  4. 德国波茨坦马克斯普朗克胶体与界面研究所

    佐尔坦·康图尔

  5. 德国柏林 Bundesanstalt für Materialforschung und-prüfung (BAM) 分析化学系 (Dpt.1)

    佐尔坦·康图尔

  6. 荷兰奈梅亨 Radboud 大学医学中心实验风湿病学系

    Debbie M. Mulder & Marije I. Koenders

  7. 瑞典斯德哥尔摩卡罗林斯卡大学医院卡罗林斯卡医学院 Solna 医学系风湿病科

    Vijay Joshua、Aase Hensvold 和 Anca I. Catrina

  8. 风湿病中心，免疫学和微生物科学学院，生命科学与医学学院，伦敦国王学院，伦敦，英国

    安德鲁·P·科普

  9. 美国宾夕法尼亚州匹兹堡匹兹堡大学医学院免疫学系

    马克·J·施洛姆奇克

  10. 德国慕尼黑路德维希马克西米利安大学医院肾脏病中心医疗诊所和诊所 IV

    汉斯-约阿希姆·安德斯

  11. 瑞典斯德哥尔摩卫生区风湿病学中心学术专家中心

    阿斯·亨斯沃尔德

  12. 瑞典乌普萨拉乌普萨拉大学免疫学、遗传学和病理学系

    约翰·罗内利德

  13. 维也纳医科大学风湿病学部，维也纳，奥地利

    君特·施泰纳

  14. Ludwig Boltzmann 关节炎和康复集群，奥地利维也纳

    君特·施泰纳

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与卡尔·斯克林纳的通信。

附加文件1：

图 1. hnRNP-D 和 hnRNP-DL 的序列、结构和主要免疫原性区域 (mir)。A，hnRNP-D（同种型 p45）、hnRNP-DL 和不同重组 hnRNP-DL 变体的示意图。突出了主要结构特征。Mir 区是主要的免疫原性区域，RBD1 和 RBD2 是 RNA 结合域 1 和 2，富含 Gly 是蛋白质的 C 端富含甘氨酸的区域。B，hnRNP-D和hnRNP-DL1（同种型1）的全局氨基酸序列比对。HnRNP-D 和 -DL 通过序列 e[1] 共享 89.1% 的相似性。区域“mir”、“RBD1”、“RBD2”和“Gly-rich”突出显示。图 2。针对 A、瓜氨酸化 α-hnRNP-DLmir (cit-DL)、B、α-hnRNP-DLmir (DL) 和 C 的自身抗体的表征，通过 ELISA 在其他疾病的血清中测定的 cit-DL 和 DL 之间的 ΔOD (ΔDL) (n=127; MS n=20, reA n=7, Sclero n=20, Sjö n=20, PsA n=20, MB n=20, OA n=20)。虚线标记了与其他疾病（系统性红斑狼疮除外）或健康对照的截断值，每个对照具有 98% 的特异性。OD，光密度；nm，纳米；对，对；MS，多发性硬化症；reA，反应性关节炎；硬皮病，硬皮病；Sjö，Sjögren 综合征；PsA，银屑病关节炎；MB，强直性脊柱炎；OA。骨关节炎。表 1. RA 队列血清阳性和血清阴性数据集的 (cit) α-hnRNP-DLmir-OD 信号的 Mann Whitney U 检验。表 2。RA 队列血清阴性数据集和其他炎症性疾病数据集的 cit α-hnRNP-DLmir-OD 信号的 Mann Whitney U 检验。图 3.早期 RA 队列 EIRA（A/D；n=404）、血清阳性 EIRA 血清（B/E；n=202）的瓜氨酸化或天然 α-hnRNP-DLmir 与 ΔhnRNP-DLmir 的 XY 图和 Spearman 相关性）和血清阴性 EIRA 血清（C/F；n=202）。表 3. EIRA 队列（n=404）早期 RA 血清的 Spearman 相关性。结果以 R 值（斜线左侧）和相应的 p 值（斜线右侧）给出。表 4.用 MTX 处理的 242 份 EIRA 血清的 Spearman 相关性（α-CCP2 阳性 n=133，α-CCP2 阴性 n=109）。结果以 R 值（斜线左侧）和相应的 p 值（斜线右侧）给出。表 5.已建立的预测队列 RA 血清的 Spearman 相关性（n=94；RF IgM 和/或 α-CCP2 阳性 n=64，RF IgM 和 α-CCP2 阴性 n=30）。结果以 R 值（斜线左侧）和相应的 p 值（斜线右侧）给出。表 6. MTX 治疗的 EIRA 患者（n=192；血清阳性 n=93，血清阴性 n=99）的天然 hnRNP-DLmir 的 ROC 分析。表 7. MTX 治疗的 EIRA 患者的负 CNDL 指数 n=192（相应的 n=161，非相应的 n=31）。表 8. Enbrel® 治疗的 Predict 患者（n=94；血清阳性 n=63，血清阴性 n=31）的天然 hnRNP-DLmir 的 ROC 分析。图 4。在接受 MTX 或 α-TNF 抑制剂治疗 (Enbrel®) 的 6 个月 EULAR Responder RA 患者中，针对 α-hnRNP-DLmir (DL) 的高基线滴度相当存在。AC、瓜氨酸化 α-hnRNP-DLmir (citDL) (A)、α-hnRNP-DLmir (DL) (B) 和 citDL 和 DL 之间的 ΔOD (ΔDL) (C) 通过 ELISA 在来自 EIRA 队列的患者血清中测量用 MTX (n=192) 治疗，6 个月内有 161 个 EULAR 响应者和 31 个 EULAR 非响应者。根据与其他疾病相比的临界值进行评估。D，α-DL 是通过 ELISA 在来自接受 α-TNF 抑制剂治疗的预测队列的患者血清中测量的，具有 6 个月的 EULAR 反应数据（n = 94，反应者 n = 63，非反应者 n = 31）。根据信号，确定响应截止值（虚线，OD 0.174），从中仅将响应者识别为阳性。OD，光密度；nm，纳米；RA，类风湿关节炎; SLE，系统性红斑狼疮；MTX，甲氨蝶呤；相应地，6 个月的 EULAR 响应者。图 5. A，通过免疫印迹测定的细胞因子对 hnRNP-DL 表达的影响。来自未刺激、IL1α 或 TNFα 刺激的 HeLa 细胞以及来自未刺激和 IL6 刺激的 HepG2 细胞的细胞提取物用 α-hnRNP-DL1/2-肽特异性兔血清进行探测。B，使用α-脱亚胺精氨酸抗体和α-hnRNP-DL抗体研究类风湿性关节炎患者滑膜组织中hnRNP-DL的瓜氨酸化。两个阳性条带都用 hnRNP-DL 标记，未分析其同种型。

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Marklein, B.、Jenning, M.、Konthur, Z.等。更正：针对 hnRNP-DL 的自身抗体的瓜氨酸化/天然指数预测了 RA 患者的个体“治疗成功窗口”。关节炎研究 23, 255 (2021)。https://doi.org/10.1186/s13075-021-02639-z

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