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The role of T helper type 17 cells in inflammatory arthritis

dc.contributor.authorSarkar, S.en_US
dc.contributor.authorCooney, L. A.en_US
dc.contributor.authorFox, D. A.en_US
dc.date.accessioned2010-06-01T22:27:34Z
dc.date.available2010-06-01T22:27:34Z
dc.date.issued2010-03en_US
dc.identifier.citationSarkar, S.; Cooney, L. A.; Fox, D. A. (2010). "The role of T helper type 17 cells in inflammatory arthritis." Clinical & Experimental Immunology 159(3): 225-237. <http://hdl.handle.net/2027.42/75449>en_US
dc.identifier.issn0009-9104en_US
dc.identifier.issn1365-2249en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/75449
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=19758374&dopt=citationen_US
dc.description.abstractWhile T cells have been implicated in the pathogenesis of inflammatory arthritis for more than three decades, the focus on the T helper type 17 (Th17) subset of CD4 T cells and their secreted cytokines, such as interleukin (IL)-17, is much more recent. Proinflammatory actions of IL-17 were first identified in the 1990s, but the delineation of a distinct Th17 subset in late 2005 has sparked great interest in the role of these cells in a broad range of immune-mediated diseases. This review summarizes current understanding of the role of Th17 cells and their products in both animal models of inflammatory arthritis and human immune-driven arthritides.en_US
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dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Publishing Ltden_US
dc.rightsJournal Compilation © 2010 British Society for Immunologyen_US
dc.subject.otherCollagen Arthritisen_US
dc.subject.otherCytokinesen_US
dc.subject.otherRheumatoid Arthritisen_US
dc.subject.otherSpondyloarthritisen_US
dc.subject.otherT Lymphocytesen_US
dc.titleThe role of T helper type 17 cells in inflammatory arthritisen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelMicrobiology and Immunologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumProgram in Immunology and Rheumatic Diseases Research Core Center, University of Michigan Division of Rheumatology, Ann Arbor, MI, USAen_US
dc.contributor.affiliationother* Department of Medicine, Section of Rheumatology, University of Arizona Tucson, AZ, anden_US
dc.identifier.pmid19758374en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/75449/1/j.1365-2249.2009.04016.x.pdf
dc.identifier.doi10.1111/j.1365-2249.2009.04016.xen_US
dc.identifier.sourceClinical & Experimental Immunologyen_US
dc.identifier.citedreferenceLubberts E, Joosten LAB, Oppers B et al. IL-1-independent role of IL-17 in synovial inflammation and joint destruction during collagen-induced arthritis. J Immunol 2001; 167: 1004 – 13.en_US
dc.identifier.citedreferenceFujimoto M, Serada S, Mihara M et al. IL-6 blockade suppresses autoimmune arthritis in mice by the inhibition of inflammatory Th17 responses. Arthritis Rheum 2008; 58: 3710 – 19.en_US
dc.identifier.citedreferenceNakae S, Nambu A, Sudo K, Iwakura Y. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol 2003; 171: 6173 – 7.en_US
dc.identifier.citedreferenceLubberts E, Koenders MI, Oppers-Walgreen B et al. Treatment with a neutralizing anti-murine IL-17 antibody after the onset of collagen-induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion. Arthritis Rheum 2004; 50: 650 – 9.en_US
dc.identifier.citedreferenceBush KA, Farmer KM, Walker JS, Kirkham BW. Reduction of joint inflammation and bone erosion in rat adjuvant arthritis by treatment with IL-17 receptor IgG1 Fc fusion protein. Arthritis Rheum 2002; 46: 802 – 5.en_US
dc.identifier.citedreferenceLubberts E, van den Bersselaar L, Oppers-Walgreen B et al. IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-κB ligand/osteoprotegerin balance. J Immunol 2003; 170: 2655 – 62.en_US
dc.identifier.citedreferenceLundy S, Sarkar S, Tesmer L, Fox D. Cells of the synovium in rheumatoid arthritis. T lymphocytes. Arthritis Res Ther 2007; 9: 202.en_US
dc.identifier.citedreferenceKuruvilla A, Shah R, Hochwald GM, Liggitt HD, Palladino MA, Thorbecke GJ. Protective effect of TGFβ1 on experimental autoimmune diseases in mice. Proc Natl Acad Sci USA 1991; 88: 2918 – 21.en_US
dc.identifier.citedreferenceThorbecke GJ, Shar R, Leu CH, Kuruvilla AP, Hardison AM, Palladino MA. Involvement of endogenous TGFα and TGFβ during induction of collagen type II arthritis in mice. Proc Natl Acad Sci USA 1992; 89: 7375 – 9.en_US
dc.identifier.citedreferenceFava R, Olsen N, Postlethwaite AE et al. Transforming growth factor beta 1 (TGFβ1) induced neutrophil recruitment to synovial tissues: implications for TGFβ-driven synovial inflammation and hyperplasia. J Exp Med 1991; 173: 1121 – 32.en_US
dc.identifier.citedreferenceCooper WO, Fava RA, Gates CA, Cremer MA, Townes AS. Acceleration of onset of collagen-induced arthritis by intra-articular injection of tumour necrosis factor or TGF β. Clin Exp Immunol 1992; 89: 244 – 50.en_US
dc.identifier.citedreferenceAllen JB, Matheny CL, Hand AR, Ohura K, Ellingsworth L, Wahl SM. Rapid onset synovial inflammation and hyperplasia induced by TGF β. J Exp Med 1990; 171: 231 – 47.en_US
dc.identifier.citedreferenceWahl SM, Allen JB, Costa GL, Wong HL, Dasch JR. Reversal of acute and chronic synovial inflammation by anti-TGF β. J Exp Med 1993; 177: 225 – 30.en_US
dc.identifier.citedreferenceEmery P, Keystone E, Tony HP et al. IL-6 receptor inhibition with tocilizumab improves treatment outcomes in patients with rheumatoid arthritis refractory to anti-tumour necrosis factor biologicals: results from a 24-week multicentre randomised placebo-controlled trial. Ann Rheum Dis 2008; 67: 1516 – 23.en_US
dc.identifier.citedreferenceNishimoto N, Miyasaka N, Yamamoto K et al. Study of active controlled tocilizumab monotherapy for rheumatoid arthritis patients with an inadequate response to methotrexate (SATORI): significant reduction in disease activity and serum vascular endothelial growth factor by IL-6 receptor inhibition therapy. Mod Rheumatol 2009; 19: 12 – 9.en_US
dc.identifier.citedreferenceNishimoto N, Hashimoto J, Miyasaka N et al. Study of active controlled monotherapy used for rheumatoid arthritis, an IL-6 inhibitor (SAMURAI): evidence of clinical and radiographic benefit from an x ray reader-blinded randomised controlled trial of tocilizumab. Ann Rheum Dis 2007; 66: 1162 – 7.en_US
dc.identifier.citedreferenceLiang B, Song Z, Wu B et al. Evaluation of anti-IL-6 monoclonal antibody therapy using murine type II collagen-induced arthritis. J Inflamm 2009; 6: 10.en_US
dc.identifier.citedreferenceNowell MA, Williams AS, Carty SA et al. Therapeutic targeting of IL-6 trans signaling counteracts STAT3 control of experimental inflammatory arthritis. J Immunol 2009; 182: 613 – 22.en_US
dc.identifier.citedreferenceAlonzi T, Fattori E, Lazzaro D et al. IL-6 is required for the development of collagen-induced arthritis. J Exp Med 1998; 187: 461 – 8.en_US
dc.identifier.citedreferenceKorn T, Bettelli E, Gao W et al. IL-21 initiates an alternative pathway to induce proinflammatory TH17 cells. Nature 2007; 448: 484 – 7.en_US
dc.identifier.citedreferenceLettesjÖ H, NordstrÖm E, StrÖm H et al. Synovial fluid cytokines in patients with rheumatoid arthritus or other arthritic lesions. Scand J Immunol 1998; 48: 286 – 92.en_US
dc.identifier.citedreferenceTran CN, Lundy SK, White PT et al. Molecular interactions between T cells and fibroblast-like synoviocytes: role of membrane TNFα on cytokine-activated T cells. Am J Pathol 2007; 171: 1588 – 98.en_US
dc.identifier.citedreferenceHwang S-Y, Kim J-Y, Kim K-W et al. IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-κB- and PI3-kinase/Akt-dependent pathways. Arthritis Res Ther 2004; 6: R120 – 8.en_US
dc.identifier.citedreferenceZhou L, Ivanov II, Spolski R et al. IL-6 programs TH-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways. Nat Immunol 2007; 8: 967 – 74.en_US
dc.identifier.citedreferenceWei L, Laurence A, Elias KM, O'Shea JJ. IL-21 is produced by Th17 cells and drives IL-17 production in a STAT3-dependent manner. J Biol Chem 2007; 282: 34605 – 10.en_US
dc.identifier.citedreferenceNurieva R, Yang XO, Martinez G et al. Essential autocrine regulation by IL-21 in the generation of inflammatory T cells. Nature 2007; 448: 480 – 3.en_US
dc.identifier.citedreferenceSpolski R, Leonard WJ. Interleukin-21: basic biology and implications for cancer and autoimmunity. Annu Rev Immunol 2008; 26: 57 – 79.en_US
dc.identifier.citedreferenceYoung DA, Hegen M, Ma HL et al. Blockade of the interleukin-21/interleukin-21 receptor pathway ameliorates disease in animal models of rheumatoid arthritis. Arthritis Rheum 2007; 56: 1152 – 63.en_US
dc.identifier.citedreferenceJang E, Cho S-H, Park H, Paik D-J, Kim JM, Youn J. A positive feedback loop of IL-21 signaling provoked by homeostatic CD4+CD25– T cell expansion is essential for the development of arthritis in autoimmune K/BxN mice. J Immunol 2009; 182: 4649 – 56.en_US
dc.identifier.citedreferenceMurphy CA, Langrish CL, Chen Y et al. Divergent pro- and anti-inflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J Exp Med 2003; 198: 1951 – 7.en_US
dc.identifier.citedreferenceChu C-Q, Swart D, Alcorn D, Tocker J, Elkon KB. IFNγ regulates susceptibility to collagen-induced arthritis through suppression of interleukin-17. Arthritis Rheum 2007; 56: 1145 – 51.en_US
dc.identifier.citedreferenceIrmler IM, Gajda M, Brauer R. Exacerbation of antigen-induced arthritis in IFNγ-deficient mice as a result of unrestricted IL-17 response. J Immunol 2007; 179: 6228 – 36.en_US
dc.identifier.citedreferenceJu JH, Cho M-L, Moon Y-M et al. IL-23 induces receptor activator of NF-κB ligand expression on CD4+ T cells and promotes osteoclastogenesis in an autoimmune arthritis model. J Immunol 2008; 181: 1507 – 18.en_US
dc.identifier.citedreferenceChen L, Wei X, Evans B, Jiang W, Aeschlimann D. IL-23 promotes osteoclast formation by up-regulation of receptor activator of NF-κB (RANK) expression in myeloid precursor cells. Eur J Immunol 2008; 38: 2845 – 54.en_US
dc.identifier.citedreferenceGoldberg M, Nadiv O, Luknar-Gabor N, Agar G, Beer Y, Katz Y. Synergism between TNFα and IL-17 to induce IL-23 p19 expression in fibroblast-like synoviocytes. Mol Immunol 2009; 46: 1854 – 9.en_US
dc.identifier.citedreferenceYago T, Nanke Y, Kawamoto M et al. IL-23 induces human osteoclastogenesis via IL-17 in vitro, and anti-IL-23 antibody attenuates collagen-induced arthritis in rats. Arthritis Res Ther 2007; 9: R96.en_US
dc.identifier.citedreferenceKotloski NJ, Nardelli DT, Peterson SH et al. IL-23 is required for development of arthritis in mice vaccinated and challenged with Borrelia species. Clin Vaccine Immunol 2008; 15: 1199 – 207.en_US
dc.identifier.citedreferenceNakae S, Saijo S, Horai R, Sudo K, Mori S, Iwakura Y. IL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist. Proc Natl Acad Sci USA 2003; 100: 5986 – 90.en_US
dc.identifier.citedreferenceKoenders MI, Devesa I, Marijnissen RJ et al. IL-1 drives pathogenic Th17 cells during spontaneous arthritis in IL-1 receptor antagonist-deficient mice. Arthritis Rheum 2008; 58: 3461 – 70.en_US
dc.identifier.citedreferenceCho M-L, Kang J-W, Moon Y-M et al. STAT3 and NF-κB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice. J Immunol 2006; 176: 5652 – 61.en_US
dc.identifier.citedreferenceHata H. Distinct contribution of IL-6, TNFα, IL-1, and IL-10 to T cell mediated spontaneous autoimmune arthritis in mice. J Clin Invest 2004; 114: 582 – 8.en_US
dc.identifier.citedreferenceHirota K, Hashimoto M, Yoshitomi H et al. T cell self-reactivity forms a cytokine milieu for spontaneous development of IL-17+ Th cells that cause autoimmune arthritis. J Exp Med 2007; 204: 41 – 7.en_US
dc.identifier.citedreferenceHirota K, Yoshitomi H, Hashimoto M et al. Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. J Exp Med 2007; 204: 2803 – 12.en_US
dc.identifier.citedreferenceYamazaki T, Yang XO, Chung Y et al. CCR6 regulates the migration of inflammatory and regulatory T cells. J Immunol 2008; 181: 8391 – 401.en_US
dc.identifier.citedreferenceKoenders MI, Kolls JK, Oppers-Walgreen B et al. IL-17 receptor deficiency results in impaired synovial expression of IL-1 and matrix metalloproteinases 3, 9, and 13 and prevents cartilage destruction during chronic reactivated streptococcal cell wall-induced arthritis. Arthritis Rheum 2005; 52: 3239 – 47.en_US
dc.identifier.citedreferenceLubberts E, Schwarzenberger P, Huang W et al. of IL-17 receptor signaling in radiation-resistant cells in the joint for full progression of destructive synovitis. J Immunol 2005; 175: 3360 – 8.en_US
dc.identifier.citedreferenceKoenders MI, Lubberts E, Oppers-Walgreen B et al. Induction of cartilage damage by overexpression of T cell IL-17A in experimental arthritis in mice deficient in IL-1. Arthritis Rheum 2005; 52: 975 – 83.en_US
dc.identifier.citedreferenceJoosten LA, Helsen M, van de Loo FA, van den Berg WB. Anticytokine treatment of established type II collagen-induced arthritis in DBA/1 mice: a comparative study using anti-TNFα, anti-IL-1α/β and IL-1Ra. Arthritis Rheum 2008; 58: S110 – S22.en_US
dc.identifier.citedreferenceJoosten LA, Abdollahi-Roodsaz S, Heuvelmans-Jacobs M et al. cell dependence of chronic destructive murine arthritis induced by repeated local activation of toll-like receptor-driven pathways: crucial role of both IL-1β and IL-17. Arthritis Rheum 2008; 58: 98 – 108.en_US
dc.identifier.citedreferenceKoenders MI, Lubberts E, van de Loo FAJ et al. IL-17 acts independently of TNFα under arthritic conditions. J Immunol 2006; 176: 6262 – 9.en_US
dc.identifier.citedreferenceNotley CA, Inglis JJ, Alzabin S, McCann FE, McNamee KE, Williams RO. Blockade of tumor necrosis factor in collagen-induced arthritis reveals a novel immunoregulatory pathway for Th1 and Th17 cells. J Exp Med 2008; 205: 2491 – 7.en_US
dc.identifier.citedreferenceDoodes PD, Cao Y, Hamel KM et al. Development of proteoglycan-induced arthritis is independent of IL-17. J Immunol 2008; 181: 329 – 37.en_US
dc.identifier.citedreferenceCao Y, Doodes PD, Glant TT, Finnegan A. IL-27 induces a Th1 immune response and susceptibility to experimental arthritis. J Immunol 2008; 180: 922 – 30.en_US
dc.identifier.citedreferenceNiedbala W, Cai B, Wei X et al. IL-27 attenuates collagen-induced arthritis. Ann Rheum Dis 2008; 67: 1474 – 9.en_US
dc.identifier.citedreferencePage G, Sattler A, Kersten S, Thiel A, Radbruch A, Miossec P. Plasma cell-like morphology of Th1-cytokine-producing cells associated with the loss of CD3 expression. Am J Pathol 2004; 164: 409 – 17.en_US
dc.identifier.citedreferenceChabaud M, Durand JM, Buchs N et al. IL-17: a T cell-derived proinflammatory cytokine produced by the rheumatoid synovium. Arthritis Rheum 1999; 42: 963 – 70.en_US
dc.identifier.citedreferenceKotake S, Udagawa N, Takahashi N et al. IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J Clin Invest 1999; 103: 1345 – 52.en_US
dc.identifier.citedreferenceZiolkowska M, Koc A, Luszczykiewicz G et al. High levels of IL-17 in rheumatoid arthritis patients: IL-15 triggers in vitro IL-17 production via cyclosporin A-sensitive mechanism. J Immunol 2000; 164: 2832 – 8.en_US
dc.identifier.citedreferenceZrioual S, Ecochard R, Tournadre A, Lenief V, Cazalis MA, Miossec P. Genome-wide comparison between IL-17A- and IL-17F-induced effects in human rheumatoid arthritis synoviocytes. J Immunol 2009; 182: 3112 – 20.en_US
dc.identifier.citedreferenceShahrara S, Huang Q, Mandelin AM II, Pope RM. TH-17 cells in rheumatoid arthritis. Arthritis Res Ther 2008; 10: R93.en_US
dc.identifier.citedreferenceJandus C, Bioley G, Rivals JP, Dudler J, Speiser D, Romero P. Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides. Arthritis Rheum 2008; 58: 2307 – 17.en_US
dc.identifier.citedreferenceHwang SY, Kim H. Expression of IL-17 homologs and their receptors in the synovial cells of rheumatoid arthritis patients. Mol Cells 2005; 19: 180 – 4.en_US
dc.identifier.citedreferenceShen H, Goodall JC, Hill Gaston JS. Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum 2009; 60: 1647 – 56.en_US
dc.identifier.citedreferenceKirkham BW, Lassere MN, Edmonds JP et al. Synovial membrane cytokine expression is predictive of joint damage progression in rheumatoid arthritis: a two-year prospective study (the DAMAGE study cohort). Arthritis Rheum 2006; 54: 1122 – 31.en_US
dc.identifier.citedreferenceAcosta-Rodriguez EV, Rivino L, Geginat J et al. Surface phenotype and antigenic specificity of human IL-17-producing T helper memory cells. Nat Immunol 2007; 8: 639 – 46.en_US
dc.identifier.citedreferenceManel N, Unutmaz D, Littman DR. The differentiation of human Th17 cells requires TGFβ and induction of the nuclear receptor RORγt. Nat Immunol 2008; 9: 641 – 9.en_US
dc.identifier.citedreferenceVolpe E, Servant N, Zollinger R et al. A critical function for TGFβ, IL-23 and proinflammatory cytokines in driving and modulating human Th17 responses. Nat Immunol 2008; 9: 650 – 7.en_US
dc.identifier.citedreferenceWilson NJ, Boniface K, Chan JR et al. Development, cytokine profile and function of human IL-17-producing helper T cells. Nat Immunol 2007; 8: 950 – 7.en_US
dc.identifier.citedreferencevan Beelen A, Zelinkova A, Taanman-Kueter E et al. Stimulation of the intracellular bacterial sensor NOD2 programs dendritic cells to promote IL-17 production in human memory T cells. Immunity 2007; 27: 660 – 9.en_US
dc.identifier.citedreferenceCosmi L, De Palma R, Santarlasci V et al. Human IL-17-producing cells originate from a CD161+CD4+ T cell precursor. J Exp Med 2008; 205: 1903 – 16.en_US
dc.identifier.citedreferenceNakae S, Iwakura Y, Suto H, Galli SJ. Phenotypic differences between Th1 and Th17 cells and negative regulation of Th1 cell differentiation by IL-17. J Leukoc Biol 2007; 81: 1258 – 68.en_US
dc.identifier.citedreferenceDeknuydt F, Bioley G, Valmori D, Ayyoub M. IL-1β and IL-2 convert human Treg into Th17 cells. Clin Immunol 2009; 131: 298 – 307.en_US
dc.identifier.citedreferenceChabaud M, Page G, Miossec P. Enhancing effect of IL-1, IL-17, and TNFα on macrophage inflammatory protein-3α production in rheumatoid arthritis: regulation by soluble receptors and Th2 cytokines. J Immunol 2001; 167: 6015 – 20.en_US
dc.identifier.citedreferenceBrennan FM, Hayes AL, Ciesielski CJ, Green P, Foxwell BMJ, Feldmann M. Evidence that rheumatoid arthritis synovial T cells are similar to cytokine-activated T cells: involvement of phosphatidylinositol 3-kinase and NF-κB pathways in TNFα production in rheumatoid arthritis. Arthritis Rheum 2002; 46: 31 – 41.en_US
dc.identifier.citedreferenceYamamura Y, Gupta R, Morita Y et al. Effector function of resting T cells: activation of synovial fibroblasts. J Immunol 2001; 166: 2270 – 5.en_US
dc.identifier.citedreferenceTsai C, Diaz LJ, Singer NG et al. Responsiveness of human T lymphocytes to bacterial superantigens presented by cultured rheumatoid arthritis synoviocytes. Arthritis Rheum 1996; 39: 125 – 36.en_US
dc.identifier.citedreferenceStanley KT, VanDort C, Motyl C, Endres J, Fox DA. Immunocompetent properties of human osteoblasts: interactions with T lymphocytes. J Bone Min Res 2006; 21: 29 – 36.en_US
dc.identifier.citedreferenceYao Z, Spriggs MK, Derry JMJ et al. Molecular characterization of the human IL-17 receptor. Cytokine 1997; 9: 794 – 800.en_US
dc.identifier.citedreferenceToy D, Kugler D, Wolfson M et al. Edge: IL-17 signals through a heteromeric receptor complex. J Immunol 2006; 177: 36 – 9.en_US
dc.identifier.citedreferenceZrioual S, Toh ML, Tournadre A et al. IL-17RA and IL-17RC receptors are essential for IL-17A-induced ELR+ CXC chemokine expression in synoviocytes and are overexpressed in rheumatoid blood. J Immunol 2008; 180: 655 – 63.en_US
dc.identifier.citedreferenceKim HR, Cho ML, Kim KW et al. Up-regulation of IL-23p19 expression in rheumatoid arthritis synovial fibroblasts by IL-17 through PI3-kinase-, NF-κB- and p38 MAPK-dependent signalling pathways. Rheumatology 2007; 46: 57 – 64.en_US
dc.identifier.citedreferencePohlers D, Beyer A, Koczan D, Wilhelm T, Thiesen HJ, Kinne RW. Constitutive upregulation of the TGFβ pathway in rheumatoid arthritis synovial fibroblasts. Arthritis Res Ther 2007; 9: R59.en_US
dc.identifier.citedreferenceLafyatis R, Thompson NL, Remmers EF et al. TGFβ production by synovial tissues from rheumatoid patients and streptococcal cell wall arthritic rats. Studies on secretion by synovial fibroblast-like cells and immunohistologic localization. J Immunol 1989; 143: 1142 – 8.en_US
dc.identifier.citedreferenceSzekanecz Z, Haines GK, Harlow LA et al. Increased synovial expression of transforming growth factor TGFβ receptor endoglin and TGFβ1 in rheumatoid arthritis: possible interactions in the pathogenesis of the disease. Clin Immunol Immunopathol 1995; 76: 187 – 94.en_US
dc.identifier.citedreferenceChu CQ, Field M, Abney E et al. TGF-β1 in rheumatoid synovial membrane and cartilage/pannus junction. Clin Exp Immunol 1991; 86: 380 – 6.en_US
dc.identifier.citedreferenceTaketazu F, Kato M, Gobl A et al. Enhanced expression of TGFβs and TGFβ type II receptor in the synovial tissues of patients with rheumatoid arthritis. Lab Invest 1994; 70: 620 – 30.en_US
dc.identifier.citedreferenceFava R, Olsen N, Keski-Oja J, Moses H, Pincus T. Active and latent forms of TGFβ activity in synovial effusions. J Exp Med 1989; 169: 291 – 6.en_US
dc.identifier.citedreferenceQuinn JM, Itoh K, Udagawa N et al. TGFβ affects osteoclast differentiation via direct and indirect actions. J Bone Miner Res 2001; 16: 1787 – 94.en_US
dc.identifier.citedreferenceFuller K, Lean J, Bayley KE, Wani MR, Chambers TJ. A role for TGFβ1 in osteoclast differentiation and survival. J Cell Sci 2000; 113: 2445 – 53.en_US
dc.identifier.citedreferenceKaneda T, Nojima T, Nakagawa M et al. Endogenous production of TGFβ is essential for osteoclastogenesis induced by a combination of receptor activator of NF-κB ligand and macrophage-colony-stimulating factor. J Immunol 2000; 165: 4254 – 63.en_US
dc.identifier.citedreferenceHase H, Kanno Y, Kojima H, Sakurai D, Kobata T. Coculture of osteoclast precursors with rheumatoid synovial fibroblasts induces osteoclastogenesis via TGFβ -mediated down-regulation of osteoprotegerin. Arthritis Rheum 2008; 58: 3356 – 65.en_US
dc.identifier.citedreferenceCheon H, Yu SJ, Yoo DH, Chae IJ, Song GG, Sohn J. Increased expression of proinflammatory cytokines and metalloproteinase-1 by TGF-β in synovial fibroblasts from rheumatoid arthritis and normal individuals. Clin Exp Immunol 2002; 127: 547 – 52.en_US
dc.identifier.citedreferenceKim HR, Kim H, Park MK, Cho ML, Lee SH, Kim HY. The clinical role of IL-23p19 in patients with rheumatoid arthritis. Scand J Rheumatol 2007; 36: 259 – 64.en_US
dc.identifier.citedreferenceMathur AN, Chang H-C, Zisoulis DG et al. STAT3 and STAT4 direct development of IL-17-secreting Th cells. J Immunol 2007; 178: 4901 – 7.en_US
dc.identifier.citedreferenceLee HS, Remmers EF, Le JM, Kastner DL, Bae SC, Gregersen PK. Association of STAT4 with rheumatoid arthritis in the Korean population. Mol Med 2007; 13: 455 – 60.en_US
dc.identifier.citedreferenceRemmers EF, Plenge RM, Lee AT et al. STAT4 and the risk of rheumatoid arthritis and systemic lupus erythematosus. N Engl J Med 2007; 357: 977 – 86.en_US
dc.identifier.citedreferenceYang L, Anderson DE, Baecher-Allan C et al. IL-21 and TGFβ are required for differentiation of human Th17 cells. Nature 2008; 454: 350 – 2.en_US
dc.identifier.citedreferenceJungel A, Distler JH, Kurowska-Stolarska M et al. Expression of IL-21 receptor, but not ILn-21, in synovial fibroblasts and synovial macrophages of patients with rheumatoid arthritis. Arthritis Rheum 2004; 50: 1468 – 76.en_US
dc.identifier.citedreferenceLi J, Shen W, Kong K, Liu Z. IL-21 induces T-cell activation and proinflammatory cytokine secretion in rheumatoid arthritis. Scand J Immunol 2006; 64: 515 – 22.en_US
dc.identifier.citedreferenceAndersson AK, Feldmann M, Brennan FM. Neutralizing IL-21 and IL-15 inhibits pro-inflammatory cytokine production in rheumatoid arthritis. Scand J Immunol 2008; 68: 103 – 11.en_US
dc.identifier.citedreferenceKuchen S, Robbins R, Sims GP et al. Essential role of IL-21 in B cell activation, expansion, and plasma cell generation during CD4+ T cell-B cell collaboration. J Immunol 2007; 179: 5886 – 96.en_US
dc.identifier.citedreferenceMiranda-Carus M-E, Balsa A, Benito-Miguel M, Perez de Ayala C, Martin-Mola E. IL-15 and the initiation of cell contact-dependent synovial fibroblast-T lymphocyte cross-talk in rheumatoid arthritis: effect of methotrexate. J Immunol 2004; 173: 1463 – 76.en_US
dc.identifier.citedreferenceBaslund B, Tvede N, Danneskiold-Samsoe B et al. Targeting IL-15 in patients with rheumatoid arthritis: a proof-of-concept study. Arthritis Rheum 2005; 52: 2686 – 92.en_US
dc.identifier.citedreferenceIkeuchi H, Kuroiwa T, Hiramatsu N et al. Expression of IL-22 in rheumatoid arthritis: potential role as a proinflammatory cytokine. Arthritis Rheum 2005; 52: 1037 – 46.en_US
dc.identifier.citedreferenceChen Z, Tato CM, Muul L, Laurence A, O'Shea JJ. Distinct regulation of IL-17 in human T helper lymphocytes. Arthritis Rheum 2007; 56: 2936 – 46.en_US
dc.identifier.citedreferenceStrieter RM, Polverini PJ, Kunkel SL et al. The functional role of the ELR motif in CXC chemokine-mediated angiogenesis. J Biol Chem 1995; 270: 27348 – 57.en_US
dc.identifier.citedreferenceStrieter RM, Burdick MD, Gomperts BN, Belperio JA, Keane MP CXC chemokines in angiogenesis. Cytokine Growth Factor Rev 2005; 16: 593 – 609.en_US
dc.identifier.citedreferenceClark-Lewis I, Dewald B, Loetscher M, Moser B, Baggiolini M. Structural requirements for IL-8 function identified by design of analogs and CXC chemokine hybrids. J Biol Chem 1994; 269: 16075 – 81.en_US
dc.identifier.citedreferenceRyu S, Lee JH, Kim SI. IL-17 increased the production of vascular endothelial growth factor in rheumatoid arthritis synoviocytes. Clin Rheumatol 2006; 25: 16 – 20.en_US
dc.identifier.citedreferenceMatsui T, Akahoshi T, Namai R et al. Selective recruitment of CCR6-expressing cells by increased production of MIP-3 alpha in rheumatoid arthritis. Clin Exp Immunol 2001; 125: 155 – 61.en_US
dc.identifier.citedreferenceHaringman JJ, Smeets TJM, Reinders-Blankert P, Tak PP. Chemokine and chemokine receptor expression in paired peripheral blood mononuclear cells and synovial tissue of patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis. Ann Rheum Dis 2006; 65: 294 – 300.en_US
dc.identifier.citedreferenceKim K-W, Cho M-L, Kim H-R et al. Up-regulation of stromal cell-derived factor 1 (CXCL12) production in rheumatoid synovial fibroblasts through interactions with T lymphocytes: role of interleukin-17 and CD40L-CD40 interaction. Arthritis Rheum 2007; 56: 1076 – 86.en_US
dc.identifier.citedreferenceShahrara S, Pickens SR, Dorfleutner A, Pope RM. IL-17 induces monocyte migration in rheumatoid arthritis. J Immunol 2009; 182: 3884 – 91.en_US
dc.identifier.citedreferenceFossiez F, Djossou O, Chomarat P et al. T cell IL-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines. J Exp Med 1996; 183: 2593 – 603.en_US
dc.identifier.citedreferenceParsonage G, Filer A, Bik M et al. Prolonged, granulocyte-macrophage colony-stimulating factor-dependent, neutrophil survival following rheumatoid synovial fibroblast activation by IL-17 and TNF α. Arthritis Res Ther 2008; 10: R47.en_US
dc.identifier.citedreferenceFujikawa Y, Shingu M, Torisu T, Itonaga I, Masumi S. Bone resorption by tartrate-resistant acid phosphatase-positive multinuclear cells isolated from rheumatoid synovium. Rheumatology 1996; 35: 213 – 17.en_US
dc.identifier.citedreferenceGravallese EM, Goldring S. Cellular mechanisms and the role of cytokines in bone erosions in rheumatoid arthritis. Arthritis Rheum 2000; 43: 2143 – 51.en_US
dc.identifier.citedreferenceTakayanagi H, Iizuka H, Juji T et al. Involvement of receptor activator of NF-κB ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis. Arthritis Rheum 2000; 43: 259 – 69.en_US
dc.identifier.citedreferenceLacey DL, Timms E, Tan HL et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell 1998; 93: 165 – 76.en_US
dc.identifier.citedreferenceKong Y-Y, Feige U, Sarosi I et al. Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand. Nature 1999; 402: 304 – 9.en_US
dc.identifier.citedreferenceKong Y-Y, Yoshida H, Sarosi I et al. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. Nature 1999; 397: 315 – 23.en_US
dc.identifier.citedreferenceDougall WC, Glaccum M, Charrier K et al. RANK is essential for osteoclast and lymph node development. Genes Dev 1999; 13: 2412 – 24.en_US
dc.identifier.citedreferenceLi J, Sarosi I, Yan XQ et al. RANK is the intrinsic hematopoietic cell surface receptor that controls osteoclastogenesis and regulation of bone mass and calcium metabolism. Proc Natl Acad Sci USA 2000; 97: 1566 – 71.en_US
dc.identifier.citedreferenceSato K, Suematsu A, Okamoto K et al. Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction. J Exp Med 2006; 203: 2673 – 82.en_US
dc.identifier.citedreferenceMiranda-CarÚs M-E, Benito-Miguel M, Balsa A et al. Peripheral blood T lymphocytes from patients with early rheumatoid arthritis express RANKL and IL-15 on the cell surface and promote osteoclastogenesis in autologous monocytes. Arthritis Rheum 2006; 54: 1151 – 64.en_US
dc.identifier.citedreferenceHofbauer LC, Lacey DL, Dunstan CR, Spelsberg TC, Riggs BL, Khosla S. IL-1β and TNFα, but not IL-6, stimulate osteoprotegerin ligand gene expression in human osteoblastic cells. Bone 1999; 25: 255 – 9.en_US
dc.identifier.citedreferenceKoshy PJ, Henderson N, Logan C, Life PF, Cawston TE, Rowan AD. IL-17 induces cartilage collagen breakdown: novel synergistic effects in combination with proinflammatory cytokines. Ann Rheum Dis 2002; 61: 704 – 13.en_US
dc.identifier.citedreferencevan Bezooijen RL, van der Wee-Pals L, Papapoulos SE, Lowik CWGM. IL-17 synergises with TNFα to induce cartilage destruction in vitro. Ann Rheum Dis 2002; 61: 870 – 6.en_US
dc.identifier.citedreferenceWendling D, Cedoz J-P, Racadot E, Dumoulin G. Serum IL-17, BMP-7, and bone turnover markers in patients with ankylosing spondylitis. Joint Bone Spine 2007; 74: 304 – 5.en_US
dc.identifier.citedreferenceWang X, Lin Z, Wei Q, Jiang Y, Gu J. Expression of IL-23 and IL-17 and effect of IL-23 on IL-17 production in ankylosing spondylitis. Rheumatol Int 2009; 29: 1343 – 7.en_US
dc.identifier.citedreferenceWendling D, Cedoz JP, Racadot E. Serum and synovial fluid levels of p40 IL-12/23 in spondyloarthropathy patients. Clin Rheumatol 2009; 28: 187 – 90.en_US
dc.identifier.citedreferenceKrueger GG, Langley RG, Leonardi C et al. A human IL-12/23 monoclonal antibody for the treatment of psoriasis. N Engl J Med 2007; 356: 580 – 92.en_US
dc.identifier.citedreferenceCiccia F, Bombardieri M, Principato A et al. Overexpression of IL-23, but not IL-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis. Arthritis Rheum 2009; 60: 955 – 65.en_US
dc.identifier.citedreference134  Wellcome Trust Case Control Consortium (WTCCC) TA-A-ASC (TASC). Association scan of 14 500 nonsynonymous SNPs in four diseases identifies autoimmunity variants. Nat Genet 2007; 39: 1329 – 37.en_US
dc.identifier.citedreferenceRueda B, Orozco G, Raya E et al. The IL-23R Arg381Gln non-synonymous polymorphism confers susceptibility to ankylosing spondylitis. Ann Rheum Dis 2008; 67: 1451 – 4.en_US
dc.identifier.citedreferenceSingh R, Aggarwal A, Misra R. Th1/Th17 cytokine profiles in patients with reactive arthritis/undifferentiated spondyloarthropathy. J Rheumatol 2007; 34: 2285 – 90.en_US
dc.identifier.citedreferenceAgarwal S, Misra R, Aggarwal A. IL-17 levels are increased in juvenile idiopathic arthritis synovial fluid and induce synovial fibroblasts to produce proinflammatory cytokines and matrix metalloproteinases. J Rheumatol 2008; 35: 515 – 19.en_US
dc.identifier.citedreferenceNistala K, Montcrieffe H, Newton KR, Varsani H, Hunter P, Wedderburn LR. IL-17-producing T cells are enriched in the joints of children with arthritis, but have a reciprocal relationship to regulatory T cell numbers. Arthritis Rheum 2008; 58: 875 – 87.en_US
dc.identifier.citedreferenceSarkar S, Tesmer LA, Hindnavis V, Endres JL, Fox DA. IL-17 as a molecular target in immune-mediated arthritis: immunoregulatory properties of genetically modified murine dendritic cells that secrete IL-4. Arthritis Rheum 2007; 56: 89 – 100.en_US
dc.identifier.citedreferenceMorita Y, Yang J, Gupta R et al. Dendritic cells genetically engineered to express IL-4 inhibit murine collagen-induced arthritis. J Clin Invest 2001; 107: 1275 – 84.en_US
dc.identifier.citedreferenceLubberts E, Joosten LAB, Chabaud M et al. IL-4 gene therapy for collagen arthritis suppresses synovial IL-17 and osteoprotegerin ligand and prevents bone erosion. J Clin Invest 2000; 105: 1697 – 710.en_US
dc.identifier.citedreferenceSloan-Lancaster J, Genovese M, Roberson S, Van den Bosch F. Safety, tolerability and evidence of efficacy of intravenous LY2439821 in patients with rheumatoid arthritis receiving background oral DMARDS. Ann Rheum Dis 2009; 68: 123.en_US
dc.identifier.citedreferenceDurez P, Chindalore V, Wittmer B et al. AIN457, an anti-IL-17 antibody, shows good safety and induces clinical responses in patients with active rheumatoid arthritis (RA) despite methotrexate therapy in a randomized, double-blind proof-of-concept trial. Ann Rheum Dis 2009; 68: 125.en_US
dc.identifier.citedreferenceKohno M, Tsutsumi A, Matsui H et al. IL-17 gene expression in patients with rheumatoid arthritis. Mod Rheumatol 2008; 18: 15 – 22.en_US
dc.identifier.citedreferenceYamada H, Nakashima Y, Okazaki K et al. Th1 but not Th17 cells predominate in the joints of patients with rheumatoid arthritis. Ann Rheum Dis 2008; 67: 1299 – 304.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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