Cytokines in the pathogenesis of rheumatoid arthritis: New players and therapeutic targets

被引:107
作者
Alunno A. [1 ]
Carubbi F. [2 ,3 ]
Giacomelli R. [2 ]
Gerli R. [1 ]
机构
[1] University of Perugia, Rheumatology Unit, Department of Medicine, Perugia
[2] University of L'Aquila, Rheumatology Unit, Department of Biotechnological and Applied Clinical Sciences, L'Aquila
[3] Department of Medicine, ASL1 Avezzano-L'Aquila-Sulmona, L'Aquila
关键词
Chronic Immune-mediated Inflammatory Disease; Epstein Barr Virus-induced Gene (EBI3); Th17 Cell Commitment; Collagen-induced Arthritis; Disease-modifying Anti-rheumatic Drugs (DMARDs);
D O I
10.1186/s41927-017-0001-8
中图分类号
学科分类号
摘要
In recent years, the landscape of pro- and anti-inflammatory cytokines has rapidly expanded with the identification of new members proven to be involved at different extent in the pathogenesis of chronic immune mediated inflammatory diseases including rheumatoid arthritis (RA). The advance of our understanding of mediators involved in the pathogenesis of RA and in consequence, the development of novel targeted therapies is necessary to provide patients not responding to currently available strategies with novel compounds. The aim of this review article is to provide an overview on recently identified cytokines, emphasizing their pathogenic role and therapeutic potential in RA. A systematic literature review was performed to retrieve articles related to every cytokine discussed in the review. In some cases, evidence from animal models and RA patients is already consistent to move forward into drug development. In others, conflicting observation and the paucity of data require further investigations.Forty years after the discovery of IL-1, the landscape of cytokines is continuously expanding with increasing possibilities to develop novel therapeutic strategies in RA. © 2017 The Author(s).
引用
收藏
相关论文
共 134 条
[1]  
Smolen J.S., Aletaha D., McInnes I.B., Rheumatoid arthritis, Lancet, 388, pp. 2023-2038, (2016)
[2]  
Picerno V., Ferro F., Adinolfi A., Valentini E., Tani C., Alunno A., One year in review: the pathogenesis of rheumatoid arthritis, Clin Exp Rheumatol, 33, 4, pp. 551-558, (2015)
[3]  
Alghasham A., Rasheed Z., Therapeutic targets for rheumatoid arthritis: progress and promises, Autoimmunity, 47, 2, pp. 77-94, (2014)
[4]  
Moots R.J., Naisbett-Groet B., The efficacy of biologic agents in patients with rheumatoid arthritis and an inadequate response to tumour necrosis factor inhibitors: a systematic review, Rheumatology (Oxford), 51, pp. 2252-2261, (2012)
[5]  
Burska A., Boissinot M., Ponchel F., Cytokines as biomarkers in rheumatoid arthritis, Mediat Inflamm, 2014, (2014)
[6]  
Dinarello C., Arend W., Sims J., Et al., IL-1 family nomenclature, Nat Immunol, 11, (2010)
[7]  
O'Neill L.A., The interleukin-1 receptor/toll-like receptor superfamily: 10 years of progress, Immunol Rev, 226, pp. 10-18, (2008)
[8]  
Baekkevold E.S., Roussigne M., Yamanaka T., Johansen F.E., Jahnsen F.L., Amalric F., Brandtzaeg P., Erard M., Haraldsen G., Girard J.P., Molecular characterization of NF-HEV, a nuclear factor preferentially expressed in human high endothelial venules, Am J Pathol, 163, pp. 69-79, (2003)
[9]  
Cayrol C., Girard J.P., The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1, Proc Natl Acad Sci U S A, 106, pp. 9021-9026, (2009)
[10]  
Schmitz J., Owyang A., Oldham E., Song Y., Murphy E., McClanahan T.K., Zurawski G., Moshrefi M., Qin J., Li X., Gorman D.M., Bazan J.F., Kastelein R.A., IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines, Immunity, 23, pp. 479-490, (2005)