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

WANG Jie; BIAN Yingying; ZHANG Chuan; KAI Guoyin; LU Yiming

doi:10.3969/j.issn.1006-0111.2017.04.001

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Article Navigation > Journal of Pharmaceutical Practice and Service > 2017 > 35(4): 289-293

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

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

doi: 10.3969/j.issn.1006-0111.2017.04.001

1.
Department of Biochemistry Pharmacy, Second Military Medical University, Shanghai, 200433, China
2.
College of Life and Environmental Science, Shanghai Normal University, Shanghai, 200234, China
3.
College of Biological Engineering, East China University of Science and Technology, Shanghai, 200237, China

Received Date: 2017-05-31
Rev Recd Date: 2017-06-20

Abstract

The TNF-α signaling pathway is a valuable target in the therapy of autoimmune diseases. TNF-α binds to two different receptors and exerts anti-inflammatory and anti-rheumatic effects. The drugs of anti-TNF-α are widely used in rheumatoid arthritis, such as infliximab, adalimumab etc. These TNF blockers have become invaluable tools to reduce damages induced by inflammation and allow recovery of the affected tissues. Unfortunately, this therapy has some drawbacks, such as increasing the risk of infection, malignancy and the incidence rate of new auto-immune diseases. Some of these effects are caused by the unwanted abrogation of beneficial TNF signaling. Therefore, elective antagonism of TNFR is an important approach to alleviate the side effects of TNF-α antibody. The medications specifically targeting the TNFR might have better applicability and safety. In this article, research progresses of TNF-α and its receptors in the therapy of rheumatoid arthritis were reviewed.
- tumor necrosis factor alpha(TNF-α),
- tumor necrosis factor receptor(TNFR),
- rheumatoid arthritis(RA),
- drug therapy

References

[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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通讯作者: 陈斌, [email protected]

1.
沈阳化工大学材料科学与工程学院沈阳 110142

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

1. Department of Biochemistry Pharmacy, Second Military Medical University, Shanghai, 200433, China

2. College of Life and Environmental Science, Shanghai Normal University, Shanghai, 200234, China

3. College of Biological Engineering, East China University of Science and Technology, Shanghai, 200237, China

Received Date: 2017-05-31

Rev Recd Date: 2017-06-20

Key words:

Abstract: The TNF-α signaling pathway is a valuable target in the therapy of autoimmune diseases. TNF-α binds to two different receptors and exerts anti-inflammatory and anti-rheumatic effects. The drugs of anti-TNF-α are widely used in rheumatoid arthritis, such as infliximab, adalimumab etc. These TNF blockers have become invaluable tools to reduce damages induced by inflammation and allow recovery of the affected tissues. Unfortunately, this therapy has some drawbacks, such as increasing the risk of infection, malignancy and the incidence rate of new auto-immune diseases. Some of these effects are caused by the unwanted abrogation of beneficial TNF signaling. Therefore, elective antagonism of TNFR is an important approach to alleviate the side effects of TNF-α antibody. The medications specifically targeting the TNFR might have better applicability and safety. In this article, research progresses of TNF-α and its receptors in the therapy of rheumatoid arthritis were reviewed.

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Reference (30)

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

doi: 10.3969/j.issn.1006-0111.2017.04.001

Abstract

References

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通讯作者: 陈斌, [email protected]

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