Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases

被引:230
作者
Croft, Michael [1 ,2 ]
Siegel, Richard M. [3 ]
机构
[1] Univ Calif San Diego, Div Immune Regulat, La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA
[2] Univ Calif San Diego, Dept Med, La Jolla, CA 92037 USA
[3] NIAMS, Immunoregulat Sect, Autoimmun Branch, NIH, Bethesda, MD 20892 USA
关键词
TUMOR-NECROSIS-FACTOR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; COLLAGEN-INDUCED ARTHRITIS; CD4(+) T-CELLS; LIGAND 1A TL1A; FIBROBLAST-LIKE SYNOVIOCYTES; LYMPHOTOXIN-BETA-RECEPTOR; SYNOVIAL FIBROBLASTS; MONOCLONAL-ANTIBODY; CD40; LIGAND;
D O I
10.1038/nrrheum.2017.22
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
TNF blockers are highly efficacious at dampening inflammation and reducing symptoms in rheumatic diseases such as rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, and also in nonrheumatic syndromes such as inflammatory bowel disease. As TNF belongs to a superfamily of 19 structurally related proteins that have both proinflammatory and anti-inflammatory activity, reagents that disrupt the interaction between proinflammatory TNF family cytokines and their receptors, or agonize the anti-inflammatory receptors, are being considered for the treatment of rheumatic diseases. Biologic agents that block B cell activating factor (BAFF) and receptor activator of nuclear factor-kappa B ligand (RANKL) have been approved for the treatment of systemic lupus erythematosus and osteoporosis, respectively. In this Review, we focus on additional members of the TNF superfamily that could be relevant for the pathogenesis of rheumatic disease, including those that can strongly promote activity of immune cells or increase activity of tissue cells, as well as those that promote death pathways and might limit inflammation. We examine preclinical mouse and human data linking these molecules to the control of damage in the joints, muscle, bone or other tissues, and discuss their potential as targets for future therapy of rheumatic diseases.
引用
收藏
页码:217 / 233
页数:17
相关论文
共 229 条
[31]   Psoriatic arthritis and TNF inhibitors: advances on effectiveness and toxicity [J].
Caso, Francesco ;
Costa, Luisa ;
Del Puente, Antonio ;
Scarpa, Raffaele .
EXPERT OPINION ON BIOLOGICAL THERAPY, 2015, 15 (01) :1-2
[32]   Soluble TNF-like cytokine (TL1A) production by immune complexes stimulated monocytes in rheumatoid arthritis [J].
Cassatella, Marco A. ;
da Silva, Gabriela Pereira ;
Tinazzi, Ilaria ;
Facchetti, Fabio ;
Scapini, Patrizia ;
Calzetti, Federica ;
Tamassia, Nicola ;
Wei, Ping ;
Nardelli, Bernardetta ;
Roschke, Viktor ;
Vecchi, Annunciata ;
Mantovani, Alberto ;
Bambara, Lisa M. ;
Edwards, Steven W. ;
Carletto, Antonio .
JOURNAL OF IMMUNOLOGY, 2007, 178 (11) :7325-7333
[33]   TNF inhibitors - Mechanisms of action, approved and off-label indications [J].
Cessak, Grzegorz ;
Kuzawinska, Olga ;
Burda, Agnieszka ;
Lis, Krzysztof ;
Wojnar, Marcin ;
Mirowska-Guzel, Dagmara ;
Balkowiec-Iskra, Ewa .
PHARMACOLOGICAL REPORTS, 2014, 66 (05) :836-844
[34]   CD40 gene polymorphisms confer risk of Behcet's disease but not of Vogt-Koyanagi-Harada syndrome in a Han Chinese population [J].
Chen, Feilan ;
Hou, Shengping ;
Jiang, Zhengxuan ;
Chen, Yuanyuan ;
Kijlstra, Aize ;
Rosenbaum, James T. ;
Yang, Peizeng .
RHEUMATOLOGY, 2012, 51 (01) :47-51
[35]   The association of CD40 polymorphisms with CD40 serum levels and risk of systemic lupus erythematosus [J].
Chen, Jian-Ming ;
Guo, Jing ;
Wei, Chuan-Dong ;
Wang, Chun-Fang ;
Luo, Hong-Cheng ;
Wei, Ye-Sheng ;
Lan, Yan .
BMC GENETICS, 2015, 16
[36]   Paradoxical effects of targeting TNF signalling in the treatment of autoimmunity [J].
Chen, Xin ;
Oppenheim, Joost J. .
NATURE REVIEWS RHEUMATOLOGY, 2016, 12 (11) :625-626
[37]   TNFR2 Is Critical for the Stabilization of the CD4+Foxp3+ Regulatory T Cell Phenotype in the Inflammatory Environment [J].
Chen, Xin ;
Wu, Xueqiang ;
Zhou, Qiong ;
Howard, O. M. Zack ;
Netea, Mihai G. ;
Oppenheim, Joost J. .
JOURNAL OF IMMUNOLOGY, 2013, 190 (03) :1076-1084
[38]   TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis [J].
Chicheportiche, Y ;
Bourdon, PR ;
Xu, HD ;
Hsu, YM ;
Scott, H ;
Hession, C ;
Garcia, I ;
Browning, JL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (51) :32401-32410
[39]   The dinucleotide repeat polymorphism in the 3′UTR of the CD154 gene has a functional role on protein expression and is associated with systemic lupus erythematosus [J].
Citores, MJ ;
Rua-Figueroa, I ;
Rodriguez-Gallego, C ;
Durántez, A ;
García-Laorden, MI ;
Rodríguez-Lozano, C ;
Rodríguez-Pérez, JC ;
Vargas, JA ;
Pérez-Aciego, P .
ANNALS OF THE RHEUMATIC DISEASES, 2004, 63 (03) :310-317
[40]   A Novel, Blocking, Fc-Silent Anti-CD40 Monoclonal Antibody Prolongs Nonhuman Primate Renal Allograft Survival in the Absence of B Cell Depletion [J].
Cordoba, F. ;
Wieczorek, G. ;
Audet, M. ;
Roth, L. ;
Schneider, M. A. ;
Kunkler, A. ;
Stuber, N. ;
Erard, M. ;
Ceci, M. ;
Baumgartner, R. ;
Apolloni, R. ;
Cattini, A. ;
Robert, G. ;
Ristig, D. ;
Munz, J. ;
Haeberli, L. ;
Grau, R. ;
Sickert, D. ;
Heusser, C. ;
Espie, P. ;
Bruns, C. ;
Patel, D. ;
Rush, J. S. .
AMERICAN JOURNAL OF TRANSPLANTATION, 2015, 15 (11) :2825-2836