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应中央军委要求,2022年9月起,《药学实践杂志》将更名为《药学实践与服务》,双月刊,正文96页;2023年1月起,拟出版月刊,正文64页,数据库收录情况与原《药学实践杂志》相同。欢迎作者踊跃投稿!

肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展

王洁 卞莹莹 张川 开国银 陆一鸣

王洁, 卞莹莹, 张川, 开国银, 陆一鸣. 肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展[J]. 药学实践与服务, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
引用本文: 王洁, 卞莹莹, 张川, 开国银, 陆一鸣. 肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展[J]. 药学实践与服务, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
WANG Jie, BIAN Yingying, ZHANG Chuan, KAI Guoyin, LU Yiming. Research progress of TNF-α and its receptors in rheumatoid arthritis[J]. Journal of Pharmaceutical Practice and Service, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
Citation: WANG Jie, BIAN Yingying, ZHANG Chuan, KAI Guoyin, LU Yiming. Research progress of TNF-α and its receptors in rheumatoid arthritis[J]. Journal of Pharmaceutical Practice and Service, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001

肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展

doi: 10.3969/j.issn.1006-0111.2017.04.001
基金项目: 国家自然科学基金资助项目(30500093,81274162);国家科技部"重大新药创制"专项(2009ZX09103-690);上海市科委生物医药领域科技支撑项目(16431904400);上海市教委科研创新项目(14ZZ077)

Research progress of TNF-α and its receptors in rheumatoid arthritis

  • 摘要: 肿瘤坏死因子α(TNF-α)信号通路是治疗自身免疫性疾病的重要靶点。TNF-α能够结合到2个不同的受体上,通过与受体的结合发挥抗炎、抗风湿的作用。抗TNF-α的药物被广泛应用于类风湿性关节炎(RA)的治疗,如英夫利昔单抗、阿达木单抗等。其在抑制炎症引起的损伤及受损组织的恢复等方面具有重要作用,但是也会引起一定的副作用,如增加感染和恶性肿瘤的风险、引起新的自身免疫性疾病等。这些副作用可能是由于封闭了TNF-α的有益信号引起的,而选择性拮抗肿瘤坏死因子受体(tumor necrosis factor receptor,TNFR)可能是解决TNF-α抗体副作用的一个重要途径,特异性地作用于TNFR的药物具有更加广阔的实用性和安全性。针对TNF-α及其受体的药物在RA中的研究进展进行综述。
  • [1] 赵金霞,刘湘源.TNF-α拮抗剂治疗类风湿关节炎疗效预测指标的研究进展[J].中华临床医师杂志, 2010, 4(4):447-449.
    [2] Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the global burden of disease 2010 study[J]. Ann Rheum Dis, 2014, 73(7): 1323-1330.
    [3] Clement SL, Scheckel C, Stoecklin G, et al. Phosphorylation of tristetraprolin by MK2 impairs AU-rich element mRNA decay by preventing deadenylase recruitment[J]. Mol Cell Biol, 2011, 31(2): 256-266.
    [4] 江海龙, 王宁远, 陆一鸣. 肿瘤坏死因子受体选择性拮抗剂的研究进展[J]. 药学实践杂志, 2015, 33(5): 392-395.
    [5] McDermott MF, Aksentijevich I, Galon J, et al. Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes[J]. Cell, 1999, 97(1): 133-144.
    [6] Xanthoulea S, Pasparakis M, Kousteni S, et al. Tumor necrosis factor (TNF) receptor shedding controls thresholds of innate immune activation that balance opposing TNF functions in infectious and inflammatory diseases[J]. J Exp Med, 2004, 200(3): 367-376.
    [7] Grell M, Douni E, Wajant H, et al. The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kDa tumor necrosis factor receptor[J]. Cell, 1995, 83(5): 793-802.
    [8] Chan FK, Chun HJ, Zheng L, et al. A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling[J]. Science, 2000, 288(5475): 2351-2354.
    [9] Micheau O, Tschopp J. Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes[J]. Cell, 2003, 114(2): 181-190.
    [10] Fotin-Mleczek M, Henkler F, Samel D, et al. Apoptotic crosstalk of TNF receptors: TNF-R2-induces depletion of TRAF2 and IAP proteins and accelerates TNF-R1-dependent activation of caspase-8[J]. J Cell Sci, 2002, 115(13): 2757-2770.
    [11] Woo YJ, Yoon B Y, Jhun JY, et al. Regulation of B cell activating factor (BAFF) receptor expression by NF-κB signaling in rheumatoid arthritis B cells[J]. Exp Mol Med, 2011, 43(6): 350-357.
    [12] 王 宁, 邢丽华.NF-κB圈套寡脱氧核苷酸技术联合紫杉醇对肺癌血管生成的影响[J].广东医学, 2011, 32 (1): 29-31.
    [13] Volanti C, Hendrickx N, Van Lint J, et al. Distinct transduction mechanisms of cyclooxygenase 2 gene activation in tumour cells after photodynamic therapy[J]. Oncogene, 2005, 24(18): 2981-2991.
    [14] Bertolini DR, Nedwin GE, Bringman TS, et al. Stimulation of bone resorption and inhibition of bone formation in vitro by human tumour necrosis factors[J]. Nature, 1986, 319(6053): 516-518.
    [15] Arntz OJ, Geurts J, Veenbergen S, et al. A crucial role for tumor necrosis factor receptor 1 in synovial lining cells and the reticuloendothelial system in mediating experimental arthritis[J]. Arthritis Res Ther, 2010, 12(2): R61.
    [16] Mori L, Iselin S, De Libero G, et al. Attenuation of collagen-induced arthritis in 55-kDa TNF receptor type 1 (TNFR1)-IgG1-treated and TNFR1-deficient mice[J]. J Immunol, 1996, 157(7): 3178-3182.
    [17] Kontoyiannis D, Pasparakis M, Pizarro TT, et al. Impaired on/off regulation of TNF biosynthesis in mice lacking TNF AU-rich elements: implications for joint and gut-associated immunopathologies[J]. Immunity, 1999, 10(3): 387-398.
    [18] Blüml S, Scheinecker C, Smolen JS, et al. Targeting TNF receptors in rheumatoid arthritis[J]. Int Immunol, 2012, 24(5): 275-281.
    [19] Donahue KE,Gartlehner G,Jonas DE,et al. Systematic review: comparative effectiveness and harms of disease-modifying medications for rheumatoid arthritis[J]. Ann Intern Med, 2008,148(2):124-134.
    [20] Van Hauwermeiren F, Vandenbroucke RE, Libert C. Treatment of TNF mediated diseases by selective inhibition of soluble TNF or TNFR1[J]. Cytokine Growth Factor Rev, 2011, 22(5-6): 311-319.
    [21] Gomez-Reino JJ, Carmona L, Valverde VR, et al. Treatment of rheumatoid arthritis with tumor necrosis factor inhibitors may predispose to significant increase in tuberculosis risk: a multicenter active-surveillance report[J]. Arthritis Rheum, 2003, 48(8):2122-2127.
    [22] Tang W, Lu Y, Tian QY, et al. The growth factor progranulin binds to TNF receptors and is therapeutic against inflammatory arthritis in mice[J]. Science, 2011, 332(6028): 478-484.
    [23] Smitten AL, Simon TA, Hochberg MC, et al. A meta-analysis of the incidence of malignancy in adult patients with rheumatoid arthritis[J].Arthritis Res Ther, 2008, 10(2): R45.
    [24] Abásolo L, Júdez E, Descalzo M, et al. Cancer in rheumatoid arthritis: occurrence, mortality, and associated factors in a South European population[J]. Semin Arthritis Rheum, 2008, 37(6): 388-397.
    [25] Askling J, Fored CM, Brandt L, et al. Risks of solid cancers in patients with rheumatoid arthritis and after treatment with tumour necrosis factor antagonists[J]. Ann Rheum Dis, 2005, 64(10): 1421-1426.
    [26] Shibata H, Yoshioka Y, Abe Y, et al. The treatment of established murine collagen-induced arthritis with a TNFR1-selective antagonistic mutant TNF[J]. Biomaterials, 2009, 30(34): 6638-6647.
    [27] McCann FE, Perocheau DP, Ruspi G, et al. Selective tumor necrosis factor receptor I blockade is antiinflammatory and reveals immunoregulatory role of tumor necrosis factor receptor Ⅱ in collagen-induced arthritis[J]. Arthritis Rheum, 2014, 66(10): 2728-2738.
    [28] Kruppa G, Thoma B, Machleidt T, et al. Inhibition of tumor necrosis factor (TNF)-mediated NF-kappa B activation by selective blockade of the human 55-kDa TNF receptor[J]. J Immunol,1992, 148(10): 3152-3157.
    [29] Moosmayer D, Dübel S, Brocks B, et al. A single-chain TNF receptor antagonist is an effective inhibitor of TNF mediated cytotoxicity[J].Ther Immunol, 1995, 2(1): 31-40.
    [30] Saito H, Kojima T, Takahashi M, et al. A tumor necrosis factor receptor loop peptide mimic inhibits bone destruction to the same extent as anti-tumor necrosis factor monoclonal antibody in murine collagen-induced arthritis[J]. Arthritis Rheum, 2007, 56(4): 1164-1174.
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肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展

doi: 10.3969/j.issn.1006-0111.2017.04.001
    基金项目:  国家自然科学基金资助项目(30500093,81274162);国家科技部"重大新药创制"专项(2009ZX09103-690);上海市科委生物医药领域科技支撑项目(16431904400);上海市教委科研创新项目(14ZZ077)

摘要: 肿瘤坏死因子α(TNF-α)信号通路是治疗自身免疫性疾病的重要靶点。TNF-α能够结合到2个不同的受体上,通过与受体的结合发挥抗炎、抗风湿的作用。抗TNF-α的药物被广泛应用于类风湿性关节炎(RA)的治疗,如英夫利昔单抗、阿达木单抗等。其在抑制炎症引起的损伤及受损组织的恢复等方面具有重要作用,但是也会引起一定的副作用,如增加感染和恶性肿瘤的风险、引起新的自身免疫性疾病等。这些副作用可能是由于封闭了TNF-α的有益信号引起的,而选择性拮抗肿瘤坏死因子受体(tumor necrosis factor receptor,TNFR)可能是解决TNF-α抗体副作用的一个重要途径,特异性地作用于TNFR的药物具有更加广阔的实用性和安全性。针对TNF-α及其受体的药物在RA中的研究进展进行综述。

English Abstract

王洁, 卞莹莹, 张川, 开国银, 陆一鸣. 肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展[J]. 药学实践与服务, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
引用本文: 王洁, 卞莹莹, 张川, 开国银, 陆一鸣. 肿瘤坏死因子及其受体在类风湿性关节炎中的研究进展[J]. 药学实践与服务, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
WANG Jie, BIAN Yingying, ZHANG Chuan, KAI Guoyin, LU Yiming. Research progress of TNF-α and its receptors in rheumatoid arthritis[J]. Journal of Pharmaceutical Practice and Service, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
Citation: WANG Jie, BIAN Yingying, ZHANG Chuan, KAI Guoyin, LU Yiming. Research progress of TNF-α and its receptors in rheumatoid arthritis[J]. Journal of Pharmaceutical Practice and Service, 2017, 35(4): 289-293. doi: 10.3969/j.issn.1006-0111.2017.04.001
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