[1] Garcia-Montoya L, Gul H, Emery P. Recent advances in ankylosing spondylitis: understanding the disease and management. F1000Research. 2018;7.
[2] Ward MM, Deodhar A, Gensler LS, Dubreuil M. 2019 Update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network Recommendations for the Treatment of Ankylosing Spondylitis and Nonradiographic Axial Spondyloarthritis. 2019;71(10):1599-613.
[3] Haibel H, Brandt HC, Song IH, Brandt A, Listing J, Rudwaleit M, et al. No efficacy of subcutaneous methotrexate in active ankylosing spondylitis: a 16-week open-label trial. Annals of the rheumatic diseases. 2007;66(3):419-21.
[4] Ma Z, Liu X, Xu X, Jiang J, Zhou J, Wang J, et al. Safety of tumor necrosis factor-alpha inhibitors for treatment of ankylosing spondylitis. Medicine. 2017;96(25):e7145.
[5] Miao J, Zhu P. Functional Defects of Treg Cells: New Targets in Rheumatic Diseases, Including Ankylosing Spondylitis. Current Rheumatology Reports. 2018;20(5).
[6] Nie J, Li YY, Zheng SG, Tsun A, Li B. FOXP3(+) Treg Cells and Gender Bias in Autoimmune Diseases. Frontiers in immunology. 2015;6:493.
[7] Sakaguchi S, Sakaguchi N, Asano M, Itoh M, Toda M. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. Journal of immunology (Baltimore, Md : 1950). 1995;155(3):1151-64.
[8] Fontenot JD, Gavin MA, Rudensky AY. Foxp3 programs the development and function of CD4+CD25+ regulatory T cells. Nature immunology. 2003;4(4):330-6.
[9] Kmieciak M, Gowda M, Graham L, Godder K, Bear HD, Marincola FM, et al. Human T cells express CD25 and Foxp3 upon activation and exhibit effector/memory phenotypes without any regulatory/suppressor function. Journal of Translational Medicine. 2009;7(1):89.
[10] Liu W, Putnam AL, Xu-Yu Z, Szot GL, Lee MR, Zhu S, et al. CD127 expression inversely correlates with FoxP3 and suppressive function of human CD4+ T reg cells. The Journal of experimental medicine. 2006;203(7):1701-11.
[11] Analay Y, Ozcan E, Karan A, Diracoglu D, Aydin R. The effectiveness of intensive group exercise on patients with ankylosing spondylitis. Clinical rehabilitation. 2003;17(6):631-6.
[12] Karatay S, Yildirim K, Melikoglu MA, Akcay F, Senel K. Effects of dynamic exercise on circulating IGF-1 and IGFBP-3 levels in patients with rheumatoid arthritis or ankylosing spondylitis. Clinical rheumatology. 2007;26(10):1635-9.
[13] Matheny RW, Jr., Nindl BC, Adamo ML. Minireview: Mechano-growth factor: a putative product of IGF-I gene expression involved in tissue repair and regeneration. Endocrinology. 2010;151(3):865-75.
[14] Yang SY, Goldspink G. Different roles of the IGF-I Ec peptide (MGF) and mature IGF-I in myoblast proliferation and differentiation. FEBS letters. 2002;522(1-3):156-60.
[15] Bilbao D, Luciani L, Johannesson B, Piszczek A, Rosenthal N. Insulin‐like growth factor‐1 stimulates regulatory T cells and suppresses autoimmune disease. EMBO Molecular Medicine. 2014;6(11):1423-35.
[16] Tran TM, Dorris ML, Satumtira N, Richardson JA, Hammer RE, Shang J, et al. Additional human beta2-microglobulin curbs HLA-B27 misfolding and promotes arthritis and spondylitis without colitis in male HLA-B27-transgenic rats. Arthritis and rheumatism. 2006;54(4):1317-27.
[17] Taurog JD, Rival C, van Duivenvoorde LM, Satumtira N, Dorris ML, Sun M, et al. Autoimmune epididymoorchitis is essential to the pathogenesis of male-specific spondylarthritis in HLA-B27-transgenic rats. Arthritis and rheumatism. 2012;64(8):2518-28.
[18] Van Tok MN, Satumtira N, Dorris M, Pots D, Slobodin G, van de Sande MG, et al. Innate Immune Activation Can Trigger Experimental Spondyloarthritis in HLA-B27/Hubeta2m Transgenic Rats. Frontiers in immunology. 2017;8:920.
[19] Waynforth H, Flecknell P. Experimental and Surgical Technique in the Rat. 2. London: Academic Press; 1992. pp. 275–276.
[20] Brown MA, Laval SH, Brophy S, Calin A. Recurrence risk modelling of the genetic susceptibility to ankylosing spondylitis. Annals of the rheumatic diseases. 2000;59(11):883-6.
[21] Long SA, Buckner JH. CD4+FOXP3+ T regulatory cells in human autoimmunity: more than a numbers game. Journal of immunology (Baltimore, Md : 1950). 2011;187(5):2061-6.
[22] Shevach EM. Foxp3(+) T Regulatory Cells: Still Many Unanswered Questions-A Perspective After 20 Years of Study. Frontiers in immunology. 2018;9:1048.
[23] Fontenot JD, Gavin MA, Rudensky AY. Foxp3 programs the development and function of CD4+CD25+ regulatory T cells. Nature immunology. 2003;4(4):330-6.
[24] Bennett CL, Christie J, Ramsdell F, Brunkow ME, Ferguson PJ, Whitesell L, et al. The immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) is caused by mutations of FOXP3. Nature genetics. 2001;27(1):20-1.
[25] Waksman BH, Pearson CM, Sharp JT. Studies of arthritis and other lesions induced in rats by injection of mycobacterial adjuvant. II. Evidence that the disease is a disseminated immunologic response to exogenous antigen. J Immunol (1960) 85:403–17.
[26] Katz L, Piliero SJ. A study of adjuvant-induced polyarthritis in the rat with special reference to associated immunological phenomena. Ann N Y Acad Sci (1969) 147(14):517–36.10.1111/j.1749-6632.1969.tb41271.x
[27] Aizman E, Blacher E, Ben-Moshe O, Kogan T, Kloog Y, Mor A. Therapeutic effect of farnesylthiosalicylic acid on adjuvant-induced arthritis through suppressed release of inflammatory cytokines. Clin Exp Immunol (2014) 175(3):458–67.10.1111/cei.12235
[28] Bais S, Abrol N, Prashar Y, Kumari R. Modulatory effect of standardised amentoflavone isolated from Juniperus communis L. against Freund’s adjuvant induced arthritis in rats (histopathological and X ray analysis). Biomed Pharmacother (2017) 86:381–92.10.1016/j.biopha.2016.12.027
[29] Pearson CM, Waksman BH, Sharp JT. Studies of arthritis and other lesions induced in rats by injection of mycobacterial adjuvant. V. Changes affecting the skin and mucous membranes. Comparison of the experimental process with human disease. J Exp Med (1961) 113:485–510.10.1084/jem.113.3.485
[30] Wang C, Yu X, Yan Y, Yang W, Zhang S, Xiang Y, et al. Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration. Acta biochimica et biophysica Sinica. 2017;49(1):1-13.
[31] Saha P, Smith A. TNF-α (Tumor Necrosis Factor-α). Arteriosclerosis, thrombosis, and vascular biology. 2018;38(11):2542-3.
[32] S. L. Gaffen, and K. D. Liu, 'Overview of Interleukin-2 Function, Production and Clinical Applications', Cytokine, 28 (2004), 109-23.
[33] G. Tian, J. L. Li, D. G. Wang, and D. Zhou, 'Targeting Il-10 in Auto-Immune Diseases', Cell Biochem Biophys, 70 (2014), 37-49.
[34] Diefenhardt P, Nosko A, Kluger MA, Richter JV, Wegscheid C, Kobayashi Y, et al. IL-10 Receptor Signaling Empowers Regulatory T Cells to Control Th17 Responses and Protect from GN. Journal of the American Society of Nephrology : JASN. 2018;29(7):1825-37.