[1] Chang S H, Dong C. Signaling of interleukin-17 family cytokines in immunity and in-flammation[J]. Cellular signalling, 2011, 23(7): 1069-1075.[2] Gu C, Wu L, Li X. IL-17 family: Cytokines, receptors and signaling[J]. Cytokine, 2013,64(2):477-485.[3] Reynolds J M, Angkasekwinai P, Dong C. IL-17 family member cytokines: regulationand function in innate immunity[J]. Cytokine & growth factor reviews, 2010, 21(6): 413-423.[4] Dong C. Diversification of T-helper-cell lineages: finding the family root of IL-17-pr-oducingcells[J]. Nature Reviews Immunology, 2006, 6(4): 329-334.[5] Song X, Qian Y. IL-17 family cytokines mediated signaling in the pathogenesis of in-flammatory diseases[J]. Cellular signalling, 2013, 25(12): 2335-2347.[6] Rouvier E, Luciani M F, Mattei M G, et al. CTLA-8, cloned from an activated T cell,bearingAU-rich messenger RNA instability sequences, and homologous to a herpesvirus sa-imiri gene[J]. The Journal of Immunology, 1993, 150(12): 5445-5456.[7]Yao Z, Fanslow W C, Seldin M F, et al. Herpesvirus saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor[J]. Journal of immunology (Baltimore, Md.: 1950), 2011, 187(9): 4392-4402.[8] Korn T, Bettelli E, Oukka M, et al. IL-17 and Th17 Cells[J]. Annual review of immunology, 2009, 27: 485-517.[9] Yao Z, Painter S L, Fanslow W C, et al. Human IL-17: a novel cytokine derived from T cells[J]. The Journal of Immunology, 1995, 155(12): 5483-5486.[10] Iwakura Y, Ishigame H, Saijo S, et al. Functional specialization of interleukin-17 family members[J]. Immunity, 2011, 34(2): 149-162.[11] Song X, Qian Y. The activation and regulation of IL-17 receptor mediated signaling[J]. Cytokine, 2013, 62(2): 175-182.[12] Shen F, Gaffen S L. Structure–function relationships in the IL-17 receptor: implications for signal transduction and therapy[J]. Cytokine, 2008, 41(2): 92-104.[13] Park Y D, Kim Y S, Jung Y M, et al. Porphyromonas gingivalis lipopolysaccharid-e regulates interleukin (IL)-17 and IL-23 expression via SIRT1 modulation in human periodontal li- gament cells[J]. Cytokine, 2012, 60(1): 284-293.[14]. Cardoso C R, Garlet G P, Crippa G E, et al. Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease[J]. Oral microbiology and immunology, 2009, 24(1): 1-6.[15] Lester S R, Bain J L, Johnson R B, et al. Gingival concentrations of interleukin-23 and-17 at healthy sites and at sites of clinical attachment loss[J]. Journal of periodontology, 2007, 78(8): 1545-1550.[16] Adibrad M, Deyhimi P, Ganjalikhani Hakemi M, et al. Signs of the presence of Th17 cells in chronic periodontal disease[J]. Journal of periodontal research, 2012, 47(4): 525-531.[17] Allam J P, Duan Y, Heinemann F, et al. IL‐23‐producing CD68+ macrophage‐like cells predominate within an IL‐17‐polarized infiltrate in chronic periodontitis lesions[J]. Journal of clinical periodontology, 2011, 38(10): 879-886.[18] Shaker O G, Ghallab N A. IL-17 and IL-11 GCF levels in aggressive and chronic periodontitis patients: relation to PCR bacterial detection[J]. Mediators of inflammation, 2012, 2012.[19] Duarte P M, da Rocha M, Sampaio E, et al. Serum levels of cytokines in subjects with generalized chronic and aggressive periodontitis before and after non-surgical periodontal therapy: a pilot study[J]. Journal of periodontology, 2010, 81(7): 1056-1063.[20] Dutzan N, Vernal R, Vaque J P, et al. Interleukin-21 expression and its association with proinflammatory cytokines in untreated chronic periodontitis patients[J]. Journal of periodontology, 2012, 83(7): 948-954.[21] Dutzan N, Gamonal J, Silva A, et al. Over-expression of forkhead box P3 and its association with receptor activator of nuclear factor-κ B ligand, interleukin (IL)-17, IL-10 and transforming growth factor-β during the progression of chronic periodontitis[J]. Journal of clinical periodontology, 2009, 36(5): 396-403.[22] Zhao L, Zhou Y, Xu Y, et al. Effect of non-surgical periodontal therapy on the levels of Th17/Th1/Th2 cytokines and their transcription factors in Chinese chronic periodontitis patients[J]. Journal of clinical periodontology, 2011, 38(6): 509-516.[23] Cheng W C, Hughes F J, Taams L S. The presence, function and regulation of IL-17 and Th17 cells in periodontitis[J]. Journal of clinical periodontology, 2014, 41(6): 541-549.[24] Guerrini M M, Takayanagi H. The immune system, bone and RANKL[J]. Archives of biochemistry and biophysics, 2014, 561: 118-123.[25] Ohyama H, Kato-Kogoe N, Kuhara A, et al. The involvement of IL-23 and the Th17 pathway in periodontitis[J]. Journal of Dental Research, 2009, 88(7): 633-638.[26] Kim Y G, Park J W, Lee J M, et al. IL-17 inhibits osteoblast differentiation and bone regeneration in rat[J]. Archives of Oral Biology, 2014.[27] 闫秀娟, 吴晓光, 郗红, 等. 二膦酸盐干预牙槽骨吸收及其机制[J]. 国际口腔医学杂志 ISTIC, 2014 (4).[28] L?nnberg A S, Zachariae C, Skov L. Targeting of interleukin-17 in the treatment of psoriasis[J]. Clinical, cosmetic and investigational dermatology, 2014, 7: 251.[29] Patel D D, Lee D M, Kolbinger F, et al. Effect of IL-17A blockade with secukinumab in autoimmune diseases[J]. Annals of the rheumatic diseases, 2012: annrheumdis-2012-202371. |