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贝利木单克隆抗体:治疗系统性红斑狼疮的新型靶向药物

贺成美,  张奉春

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文章导航 > 协和医学杂志  > 2020 >  11(2): 130-134
贺成美, 张奉春. 贝利木单克隆抗体:治疗系统性红斑狼疮的新型靶向药物[J]. 协和医学杂志, 2020, 11(2): 130-134. doi: 10.3969/j.issn.1674-9081.20190114
引用本文: 贺成美, 张奉春. 贝利木单克隆抗体:治疗系统性红斑狼疮的新型靶向药物[J]. 协和医学杂志, 2020, 11(2): 130-134. doi: 10.3969/j.issn.1674-9081.20190114
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Cheng-mei HE, Feng-chun ZHANG. Belimumab:A New Targeted Drug for Systemic Lupus Erythematosus[J]. Medical Journal of Peking Union Medical College Hospital, 2020, 11(2): 130-134. doi: 10.3969/j.issn.1674-9081.20190114
Citation: Cheng-mei HE, Feng-chun ZHANG. Belimumab:A New Targeted Drug for Systemic Lupus Erythematosus[J]. Medical Journal of Peking Union Medical College Hospital, 2020, 11(2): 130-134. doi: 10.3969/j.issn.1674-9081.20190114
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贝利木单克隆抗体:治疗系统性红斑狼疮的新型靶向药物

doi: 10.3969/j.issn.1674-9081.20190114

  • 中国医学科学院 北京协和医学院 北京协和医院风湿免疫科, 北京 100730

详细信息
    通讯作者:

    张奉春 电话:010-69155007, E-mail:zhangfccra@aliyun.com

  • 中图分类号: R593.24;R453

Belimumab:A New Targeted Drug for Systemic Lupus Erythematosus

  • Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China

More Information

    摘要
  • 摘要: 系统性红斑狼疮(systemic lupus erythematosus, SLE)是一种复杂的自身免疫性疾病, B细胞异常活化在发病中起重要作用。贝利木单克隆抗体是一种人源化单克隆抗体, 能通过结合肿瘤坏死因子家族B细胞活化因子(B-cell-activating factor of the tumor necrosis factor family, BAFF), 减少活化B细胞的数量。2011年美国食品药品监督管理局批准贝利木单克隆抗体上市, 为SLE患者提供了新的用药选择。本文主要介绍贝利木单克隆抗体治疗机制及相关临床研究, 并对其未来进行展望。
    Abstract: Systemic lupus erythematosus(SLE) is a complicated autoimmune disease characterized by aberrant B cell activation. Belimumab is a human monoclonal antibody, which can reduce active B cells through binding to the B-cell-activating factor of the tumor necrosis factor family(BAFF). In 2011, the US Food and Drugs Administration approved belimumab as a new drug option for SLE patients. This article mainly discusses the mechanism and relevant clinical trials of belimumab and looks forward to its future.
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    • 参考文献(32)
  • [1] Tsokos GC, Lo MS, Costa Reis P, et al. New insights into the immunopathogenesis of systemic lupus erythematosus[J]. Nat Rev Rheumatol, 2016, 12:716-730. doi:  10.1038/nrrheum.2016.186
    [2] Kamal A, Khamashta M. The efficacy of novel B cell biologics as the future of SLE treatment:a review[J]. Autoimmun Rev, 2014, 13:1094-1101. doi:  10.1016/j.autrev.2014.08.020
    [3] Sanz I, Lee FE. B cells as therapeutic targets in SLE[J]. Nat Rev Rheumatol, 2010, 6:326-337. doi:  10.1038/nrrheum.2010.68
    [4] Sanz I. Rationale for B cell targeting in SLE[J]. Semin Immunopathol, 2014, 36:365-375. doi:  10.1007/s00281-014-0430-z
    [5] Schneider P, MacKay F, Steiner V, et al. BAFF, a novel ligand of the tumor necrosis factor family, stimulates B cell growth[J]. J Exp Med, 1999, 189:1747-1756. doi:  10.1084/jem.189.11.1747
    [6] Vincent FB, Saulep-Easton D, Figgett WA, et al. The BAFF/APRIL system:emerging functions beyond B cell biology and autoimmunity[J]. Cytokine Growth Factor Rev, 2013, 24:203-215. doi:  10.1016/j.cytogfr.2013.04.003
    [7] Vincent FB, Morand EF, Schneider P, et al. The BAFF/APRIL system in SLE pathogenesis[J]. Nat Rev Rheumatol, 2014, 10:365-373. doi:  10.1038/nrrheum.2014.33
    [8] Patke A, Mecklenbrauker I, Erdjument-Bromage H, et al. BAFF controls B cell metabolic fitness through a PKC beta- and Akt-dependent mechanism[J]. J Exp Med, 2006, 203:2551-2562. doi:  10.1084/jem.20060990
    [9] Kayagaki N, Yan M, Seshasayee D, et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete surface loop and promotes processing of NF-kappaB2[J]. Immunity, 2002, 17:515-524. doi:  10.1016/S1074-7613(02)00425-9
    [10] Gross JA, Dillon SR, Mudri S, et al. TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease:impaired B cell maturation in mice lacking BLyS[J]. Immunity, 2001, 15:289-302. doi:  10.1016/S1074-7613(01)00183-2
    [11] Schiemann B, Gommerman JL, Vora K, et al. An essential role for BAFF in the normal development of B cells through a BCMA-independent pathway[J]. Science, 2001, 293:2111-2114. doi:  10.1126/science.1061964
    [12] Saulep-Easton D, Vincent FB, Quah PS, et al. The BAFF receptor TACI controls IL-10 production by regulatory B cells and CLL B cells[J]. Leukemia, 2016, 30:163-172. doi:  10.1038/leu.2015.174
    [13] Ahmed SS, Wang XN, Norden J, et al. Identification and validation of biomarkers associated with acute and chronic graft versus host disease[J]. Bone Marrow Transplant, 2015, 50:1563-1571. doi:  10.1038/bmt.2015.191
    [14] Shlomchik MJ, Madaio MP, Ni D, et al. The role of B cells in lpr/lpr-induced autoimmunity[J]. J Exp Med, 1994, 180:1295-1306. doi:  10.1084/jem.180.4.1295
    [15] Yaniv G, Twig G, Shor DB, et al. A volcanic explosion of autoantibodies in systemic lupus erythematosus:a diversity of 180 different antibodies found in SLE patients[J]. Autoimmun Rev, 2015, 14:75-79. doi:  10.1016/j.autrev.2014.10.003
    [16] Vaughn SE, Kottyan LC, Munroe ME, et al. Genetic susceptibility to lupus:the biological basis of genetic risk found in B cell signaling pathways[J]. J Leukocyte Biol, 2012, 92:577-591. doi:  10.1189/jlb.0212095
    [17] Sun C, Molineros JE, Looger LL, et al. High-density genotyping of immune-related loci identifies new SLE risk variants in individuals with Asian ancestry[J]. Nat Genet, 2016, 48:323-330. doi:  10.1038/ng.3496
    [18] Steri M, Orru V, Idda ML, et al. Overexpression of the Cytokine BAFF and Autoimmunity Risk[J]. New Engl J Med, 2017, 376:1615-1626. doi:  10.1056/NEJMoa1610528
    [19] Pers JO, Daridon C, Devauchelle V, et al. BAFF overexpression is associated with autoantibody production in autoimmune diseases[J]. Ann N Y Acad Sci, 2005, 1050:34-39. doi:  10.1196/annals.1313.004
    [20] Gross JA, Johnston J, Mudri S, et al. TACI and BCMA are receptors for a TNF homologue implicated in B-cell autoimmune disease[J]. Nature, 2000, 404:995-999. doi:  10.1038/35010115
    [21] Mackay F, Woodcock SA, Lawton P, et al. Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations[J]. J Exp Med, 1999, 190:1697-1710. doi:  10.1084/jem.190.11.1697
    [22] Ding H, Wang L, Wu X, et al. Blockade of B-cell-activating factor suppresses lupus-like syndrome in autoimmune BXSB mice[J]. J Cell Mol Med, 2010, 14:1717-1725. http://europepmc.org/articles/PMC3829033/
    [23] Jacob CO, Pricop L, Putterman C, et al. Paucity of clinical disease despite serological autoimmunity and kidney pathology in lupus-prone New Zealand mixed 2328 mice deficient in BAFF[J]. J Immunol, 2006, 177:2671-2680. doi:  10.4049/jimmunol.177.4.2671
    [24] Baker KP, Edwards BM, Main SH, et al. Generation and characterization of LymphoStat-B, a human monoclonal antibody that antagonizes the bioactivities of B lymphocyte stimulator[J]. Arthritis Rheum, 2003, 48:3253-3265. doi:  10.1002/art.11299
    [25] Nakayamada S, Tanaka Y. BAFF- and APRIL-targeted therapy in systemic autoimmune diseases[J]. Inflamm Regen, 2016, 36:6. doi:  10.1186/s41232-016-0015-4
    [26] Navarra SV, Guzman RM, Gallacher AE, et al. Efficacy and safety of belimumab in patients with active systemic lupus erythematosus:a randomised, placebo-controlled, phase 3 trial[J]. Lancet, 2011, 377:721-731. doi:  10.1016/S0140-6736(10)61354-2
    [27] Furie R, Petri M, Zamani O, et al. A phase Ⅲ, randomized, placebo-controlled study of belimumab, a monoclonal antibody that inhibits B lymphocyte stimulator, in patients with systemic lupus erythematosus[J]. Arthritis Rheum, 2011, 63:3918-3930. doi:  10.1002/art.30613
    [28] Dooley MA, Houssiau F, Aranow C, et al. Effect of belimumab treatment on renal outcomes:results from the phase 3 belimumab clinical trials in patients with SLE[J]. Lupus, 2013, 22:63-72. doi:  10.1177/0961203312465781
    [29] Stohl W, Schwarting A, Okada M, et al. Efficacy and Safety of Subcutaneous Belimumab in Systemic Lupus Erythema-tosus:A Fifty-Two-Week Randomized, Double-Blind, Placebo-Controlled Study[J]. Arthritis Rheumatol, 2017, 69:1016-1027. doi:  10.1002/art.40049
    [30] Zhang F, Bae SC, Bass D, et al. A pivotal phase Ⅲ, randomised, placebo-controlled study of belimumab in patients with systemic lupus erythematosus located in China, Japan and South Korea[J]. Ann Rheum Dis, 2018, 77:355-363. doi:  10.1136/annrheumdis-2017-211631
    [31] Jordan NP, D'Cruz DP. Efficacy, pharmacokinetic and pharmacodynamic profile of belimumab for systemic lupus erythematosus[J]. Expert Opin Drug Metab Toxicol, 2015, 11:1635-1645. doi:  10.1517/17425255.2015.1077808
    [32] Ginzler EM, Wallace DJ, Merrill JT, et al. Disease control and safety of belimumab plus standard therapy over 7 years in patients with systemic lupus erythematosus[J]. J Rheumatol, 2014, 41:300-309. doi:  10.3899/jrheum.121368
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出版历程
  • 收稿日期:  2019-06-19
  • 刊出日期:  2020-03-30

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