McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365:2205–19.
O'Shea JJ, Plenge R. JAK and STAT signaling molecules in immunoregulation and immune-mediated disease. Immunity. 2012;36:542–50.
Kontzias A, Kotlyar A, Laurence A, Changelian P, O'Shea JJ. Jakinibs: a new class of kinase inhibitors in cancer and autoimmune disease. Curr Opin Pharmacol. 2012;12:464–70.
van der Heijde D, Tanaka Y, Fleischmann R, Keystone E, Kremer J, Zerbini C, et al. Tofacitinib (CP-690,550) in patients with rheumatoid arthritis receiving methotrexate: twelve-month data from a twenty-four-month phase III randomized radiographic study. Arthritis Rheum. 2013;65:559–70.
Coombs JH, Bloom BJ, Breedveld FC, Fletcher MP, Gruben D, Kremer JM, et al. Improved pain, physical functioning and health status in patients with rheumatoid arthritis treated with CP-690,550, an orally active Janus kinase (JAK) inhibitor: results from a randomised, double-blind, placebo-controlled trial. Ann Rheum Dis. 2010;69:413–6.
Lin TH, Hegen M, Quadros E, Nickerson-Nutter CL, Appell KC, Cole AG, et al. Selective functional inhibition of JAK-3 is sufficient for efficacy in collagen-induced arthritis in mice. Arthritis Rheum. 2010;62:2283–93.
Fridman JS, Scherle PA, Collins R, Burn TC, Li Y, Li J, et al. Selective inhibition of JAK1 and JAK2 is efficacious in rodent models of arthritis: preclinical characterization of INCB028050. J Immunol. 2010;184:5298–307.
LaBranche TP, Jesson MI, Radi ZA, Storer CE, Guzova JA, Bonar SL, et al. JAK inhibition with tofacitinib suppresses arthritic joint structural damage through decreased RANKL production. Arthritis Rheum. 2012;64:3531–42.
Millecamps M, Jourdan D, Leger S, Etienne M, Eschalier A, Ardid D. Circadian pattern of spontaneous behavior in monarthritic rats: a novel global approach to evaluation of chronic pain and treatment effectiveness. Arthritis Rheum. 2005;52:3470–8.
Sasakawa T, Sasakawa Y, Ohkubo Y, Mutoh S. FK506 ameliorates spontaneous locomotor activity in collagen-induced arthritis: implication of distinct effect from suppression of inflammation. Int Immunopharmacol. 2005;5:503–10.
Philippe L, Gegout-Pottie P, Guingamp C, Bordji K, Terlain B, Netter P, et al. Relations between functional, inflammatory, and degenerative parameters during adjuvant arthritis in rats. Am J Physiol. 1997;273:R1550–6.
Tanimoto A, Ogawa Y, Oki C, Kimoto Y, Nozawa K, Amano W, et al. Pharmacological properties of JTE-052: a novel potent JAK inhibitor that suppresses various inflammatory responses in vitro and in vivo. Inflamm Res. 2015;64:41–51.
Yamaguchi T, Kakefuda R, Tanimoto A, Watanabe Y, Tajima N. Suppressive effect of an orally active MEK1/2 inhibitor in two different animal models for rheumatoid arthritis: a comparison with leflunomide. Inflamm Res. 2012;61:445–54.
Randall LO, Selitto JJ. A method for measurement of analgesic activity on inflamed tissue. Arch Int Pharmacodyn Ther. 1957;111:409–19.
Yonemori F, Yamaguchi T, Nakayama H, Narita K, Hojo S, Tamura A. Effect of JTP-2942, a novel thyrotropin-releasing hormone analog, on motor deficits after chronic focal cerebral ischemia in rats. J Cereb Blood Flow Metab. 2000;20:74–81.
Balague C, Pont M, Prats N, Godessart N. Profiling of dihydroorotate dehydrogenase, p38 and JAK inhibitors in the rat adjuvant-induced arthritis model: a translational study. Br J Pharmacol. 2012;166:1320–32.
Stolina M, Schett G, Dwyer D, Vonderfecht S, Middleton S, Duryea D, et al. RANKL inhibition by osteoprotegerin prevents bone loss without affecting local or systemic inflammation parameters in two rat arthritis models: comparison with anti-TNFalpha or anti-IL-1 therapies. Arthritis Res Ther. 2009;11:R187.
Stolina M, Bolon B, Middleton S, Dwyer D, Brown H, Duryea D, et al. The evolving systemic and local biomarker milieu at different stages of disease progression in rat adjuvant-induced arthritis. J Clin Immunol. 2009;29:158–74.
Nielsen CH, Albertsen L, Bendtzen K, Baslund B. Methotrexate induces poly(ADP-ribose) polymerase-dependent, caspase 3-independent apoptosis in subsets of proliferating CD4+ T cells. Clin Exp Immunol. 2007;148:288–95.
Sfikakis PP, Souliotis VL, Panayiotidis PP. Suppression of interleukin-2 and interleukin-2 receptor biosynthesis by gold compounds in in vitro activated human peripheral blood mononuclear cells. Arthritis Rheum. 1993;36:208–12.
Lipsky PE. Immunosuppression by D-penicillamine in vitro. Inhibition of human T lymphocyte proliferation by copper- or ceruloplasmin-dependent generation of hydrogen peroxide and protection by monocytes. J Clin Invest. 1984;73:53–65.
Carlson RP, Datko LJ, O'Neill-Davis L, Blazek EM, DeLustro F, Beideman R, et al. Comparison of inflammatory changes in established type II collagen- and adjuvant-induced arthritis using outbred Wistar rats. Int J Immunopharmacol. 1985;7:811–26.
Maeshima K, Yamaoka K, Kubo S, Nakano K, Iwata S, Saito K, et al. The JAK inhibitor tofacitinib regulates synovitis through inhibition of interferon-γ and interleukin-17 production by human CD4+ T cells. Arthritis Rheum. 2012;64:1790–8.
Meyer DM, Jesson MI, Li X, Elrick MM, Funckes-Shippy CL, Warner JD, et al. Anti-inflammatory activity and neutrophil reductions mediated by the JAK1/JAK3 inhibitor, CP-690,550, in rat adjuvant-induced arthritis. J Inflamm (Lond). 2010;7:41.
Heiberg T, Kvien TK. Preferences for improved health examined in 1,024 patients with rheumatoid arthritis: pain has highest priority. Arthritis Rheum. 2002;47:391–7.
Courvoisier DS, Agoritsas T, Glauser J, Michaud K, Wolfe F, Cantoni E, et al. Pain as an important predictor of psychosocial health in patients with rheumatoid arthritis. Arthritis Care Res (Hoboken). 2012;64:190–6.
Huang J, Zhang X, McNaughton PA. Inflammatory pain: the cellular basis of heat hyperalgesia. Curr Neuropharmacol. 2006;4:197–206.
Aletaha D, Smolen J, Ward MM. Measuring function in rheumatoid arthritis: Identifying reversible and irreversible components. Arthritis Rheum. 2006;54:2784–92.
Aletaha D, Funovits J, Smolen JS. Physical disability in rheumatoid arthritis is associated with cartilage damage rather than bone destruction. Ann Rheum Dis. 2011;70:733–9.
Wolfe F, Hawley DJ, Wilson K. The prevalence and meaning of fatigue in rheumatic disease. J Rheumatol. 1996;23:1407–17.
Arend WP, Dayer JM. Inhibition of the production and effects of interleukin-1 and tumor necrosis factor alpha in rheumatoid arthritis. Arthritis Rheum. 1995;38:151–60.
Druce KL, Jones GT, Macfarlane GJ, Basu N. Patients receiving anti-TNF therapies experience clinically important improvements in RA-related fatigue: results from the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis. Rheumatology (Oxford). 2015;54:964–71.
Alten R, Gomez-Reino J, Durez P, Beaulieu A, Sebba A, Krammer G, et al. Efficacy and safety of the human anti-IL-1beta monoclonal antibody canakinumab in rheumatoid arthritis: results of a 12-week, Phase II, dose-finding study. BMC Musculoskelet Disord. 2011;12:153.
Gaffen SL. Biology of recently discovered cytokines: interleukin-17--a unique inflammatory cytokine with roles in bone biology and arthritis. Arthritis Res Ther. 2004;6:240–7.
McInnes IB, Gracie JA. Targeting cytokines beyond tumor necrosis factor-alpha and interleukin-1 in rheumatoid arthritis. Curr Rheumatol Rep. 2004;6:336–42.
Dayer JM, Choy E. Therapeutic targets in rheumatoid arthritis: the interleukin-6 receptor. Rheumatology (Oxford). 2010;49:15–24.
Lamkin DM, Lutgendorf SK, Lubaroff D, Sood AK, Beltz TG, Johnson AK. Cancer induces inflammation and depressive-like behavior in the mouse: modulation by social housing. Brain Behav Immun. 2011;25:555–64.
Murray PJ. The JAK-STAT signaling pathway: input and output integration. J Immunol. 2007;178:2623–9.