New aspects of the pathogenesis of psoriasis

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Psoriasis is a chronic multi-factorial immune-mediated inflammatory disease of skin and joints. The variety of clinical forms of dermatosis is consistent with various pathogenetic features of the disease progress which have been significantly supplemented and reviewed recently. Knowledge of these mechanisms will improve and personalize the prescribed therapy.

This study places the emphasis on modern ideas about the formation of T cell memory, the role of melanocytes and innate lymphoid cells. Development mechanisms of guttate and paradoxical psoriasis with important distinguishing characteristics are described separately.

Today, knowledge of the molecular basis of the disease progression has led to the creation and introduction of a number of highly effective targeted drugs into clinical practice. Further developments related to the inhibition of resident memory cells, innate lymphoid cells, as well as the study of guttate psoriasis perpetuation and the occurrence of paradoxical psoriasis will significantly increase the effectiveness of the therapy.

作者简介

Alexander Zhukov

S.M. Kirov Military Medical Academy

编辑信件的主要联系方式.
Email: doctor-vma@mail.ru
ORCID iD: 0000-0002-4915-9157
SPIN 代码: 4570-3470

MD, Cand. Sci. (Med.)

俄罗斯联邦, 6, Akademika Lebedeva str., Saint Petersburg, 194044

Alexander Patrushev

S.M. Kirov Military Medical Academy

Email: alexpat2@yandex.ru
ORCID iD: 0000-0002-6989-9363
SPIN 代码: 1367-5580

MD, Dr. Sci. (Med.)

俄罗斯联邦, 6, Akademika Lebedeva str., Saint Petersburg, 194044

Vladislav Khairutdinov

S.M. Kirov Military Medical Academy

Email: haric@mail.ru
ORCID iD: 0000-0002-0387-5481
SPIN 代码: 4417-9117

MD, Dr. (Sci.) Med., assistant professor

俄罗斯联邦, 6, Akademika Lebedeva str., Saint Petersburg, 194044

Alexey Samtsov

S.M. Kirov Military Medical Academy

Email: avsamtsov@mail.ru
ORCID iD: 0000-0002-9458-0872
SPIN 代码: 2287-5062

MD, Dr. (Sci.) Med, Professor

俄罗斯联邦, 6, Akademika Lebedeva str., Saint Petersburg, 194044

Evgeniy Kryukov

S.M. Kirov Military Medical Academy

Email: evgeniy.md@mail.ru
ORCID iD: 0000-0002-8396-1936
SPIN 代码: 3900-3441

MD, Dr. (Sci.) Med, Professor, Academician of the Russian Academy of Sciences

俄罗斯联邦, 6, Akademika Lebedeva str., Saint Petersburg, 194044

参考

  1. Parisi R, Symmons DP, Griffiths CE, Ashcroft DM. Identification and Management of Psoriasis and Associated ComorbidiTy (IMPACT) project team. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. J Invest Dermatol. 2013;133(2):377–385. doi: 10.1038/jid.2012.339
  2. Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017;31(2):205–212. doi: 10.1111/jdv.13854
  3. Boehncke WH, Schn MP. Psoriasis. Lancet. 2015;386(9997):983–994. doi: 10.1016/S0140-6736(14)61909-7
  4. Tsoi LC, Spain SL, Knight J, Ellinghaus E, Stuart PE, Capon F, et al. Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity. Nat Genet. 2012;44(12):1341–1348. doi: 10.1038/ng.2467.
  5. Tang H, Jin X, Li Y, Jiang H, Tang X, Yang X, et al. A large-scale screen for coding variants predisposing to psoriasis. Nat Genet. 2014;46(1):45–50. doi: 10.1038/ng.2827
  6. Chandra A, Ray A, Senapati S, Chatterjee R. Genetic and epigenetic basis of psoriasis pathogenesis. Mol Immunol. 2015;64(2):313–323. doi: 10.1016/j.molimm.2014.12.014.
  7. Gudjonsson JE, Karason A, Antonsdottir A, Runarsdottir EH, Hauksson VB, Upmanyu R, Gulcher J, Stefansson K, Valdimarsson H. Psoriasis patients who are homozygous for the HLA-Cw*0602 allele have a 2.5-fold increased risk of developing psoriasis compared with Cw6 heterozygotes. Br J Dermatol. 2003;148(2):233–235. doi: 10.1046/j.1365-2133.2003.05115.x.
  8. Nair RP, Stuart PE, Nistor I, Hiremagalore R, Chia NVC, Jenisch S, Weichenthal M, Abecasis GR, Lim HW, Christophers E, Voorhees JJ, Elder JT. Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene. Am J Hum Genet. 2006;78(5):827–851. doi: 10.1086/503821.
  9. Lonnberg AS, Skov L, Skytthe A, Kyvik KO, Pedersen OB, Thomsen SF. Heritability of psoriasis in a large twin sample. Br J Dermatol. 2013;169:412–416. doi: 10.1111/bjd.12375
  10. Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013;87(9):626–633.
  11. Kimball AB, Leonardi C, Stahle M, Gulliver W, Chevrier M, Fakharzadeh S, et al. Demography, baseline disease characteristics and treatment history of patients with psoriasis enrolled in a multicentre, prospective, disease-based registry (PSOLAR). Br J Dermatol. 2014;171(1):137–147. doi: 10.1111/bjd.13013.
  12. Mendieta KL, Irfan M, Fernandez Faith E. Interferon-alpha induced psoriasis in a teenager. Pediatr Dermatol. 2018;35(2):e136–137. doi: 10.1111/pde.13418
  13. Farber EM, Nall ML, Watson W. Natural history of psoriasis in 61 twin pairs. Arch Dermatol. 1974;109(2):207-211.
  14. Brandrup F, Hauge M, Henningsen K, Eriksen B. Psoriasis in an unselected series of twins. Arch Dermatol. 1978;114(6):874–878.
  15. Mori N, Yoshikawa K, Ohno M. Psoriasis occuring in young monozygotic twins. J Dermatol. 1980;7(1):71–73. doi: 10.1111/j.1346-8138.1980.tb01945.x
  16. Lønnberg AS, Skov L, Skytthe A, Kyvik KO, Pedersen OB, Thomsen SF. Heritability of psoriasis in a large twin sample. Br J Dermatol. 2013;169(2):412-416. doi: 10.1111/bjd.12375
  17. Nestle FO. Skin immune sentinels in health and disease. Nat Rev Immunol. 2009;9(10):679–691. doi: 10.1038/nri2622
  18. Albanesi C, Madonna S, Gisondi P, Girolomoni G. The Interplay Between Keratinocytes and Immune Cells in the Pathogenesis of Psoriasis. Front Immunol. 2018;9:1549. doi: 10.3389/fimmu.2018.01549
  19. Arakawa A, Siewert K, Stöhr J, Besgen P, Kim SM, Rühl G, et al. Melanocyte antigen triggers autoimmunity in human psoriasis. J Exp Med. 2015;212(13):2203–2212. doi: 10.1084/jem.20151093
  20. Lande R, Botti E, Jandus C, Dojcinovic D, Fanelli G, Conrad C, et al. The antimicrobial peptide LL37 is a T-cell autoantigen in psoriasis. Nat Commun. 2014;3(5):5621. doi: 10.1038/ncomms6621
  21. Cheung KL, Jarrett R, Subramaniam S, Salimi M, Gutowska-Owsiak D, Chen YL, et al. Psoriatic T cells recognize neolipid antigens generated by mast cell phospholipase delivered by exosomes and presented by CD1a. J Exp Med. 2016;213(11):2399–2412. doi: 10.1084/jem.20160258
  22. Fuentes-Duculan J, Bonifacio KM, Hawkes JE, Kunjravia N, Cueto I, Li X, et al. Autoantigens ADAMTSL5 and LL37 are significantly upregulated in active psoriasis and localized with keratinocytes, dendritic cells and other leukocytes. Exp Dermatol. 2017;26(11):1075–1082. doi: 10.1111/exd.13378
  23. Johnston A, Gudjonsson JE, Sigmundsdottir H, Love TJ, Valdimarsson H. Peripheral blood T cell responses to keratin peptides that share sequences with streptococcal M proteins are largely restricted to skin-homing CD8(+) T cells. Clin Exp Immunol. 2004;138(1):83–93. doi: 10.1111/j.1365-2249.2004.00600.x
  24. Lande R, Gregorio J, Facchinetti V, Chatterjee B, Wang YH, Homey B, Cao W, et al. Plasmacytoid dendritic cells sense self‐DNA coupled with antimicrobial peptide. Nature. 2007;449:564–569. doi: 10.1038/nature06116
  25. Kahlenberg JM, Kaplan MJ. Little peptide, big effects: the role of LL-37 in inflammation and autoimmune disease. J Immunol. 2013;191(10):4895–4901. doi: 10.4049/jimmunol.1302005
  26. Lande R, Chamilos G, Ganguly D, Demaria O, Frasca L, Durr S, et al. Cationic antimicrobial peptides in psoriatic skin cooperate to break innate tolerance to self-DNA. Eur J Immunol. 2015;45(1):203–213. doi: 10.1002/eji.201344277
  27. Dombrowski Y, Peric M, Koglin S, Kammerbauer C, Göss C Anz D, et al. Cytosolic DNA Triggers Inflammasome Activation in Keratinocytes in Psoriatic Lesions. Sci Transl Med. 2011;3(82):82ra38. doi: 10.1126/scitranslmed.3002001
  28. Paludan SR, Bowie AG. Immune sensing of DNA. Immunity. 2013;38:870–880. doi: 10.1016/j.immuni.2013.05.004
  29. Chiliveru S, Rahbek SH, Jensen SK, Jørgensen SE, Nissen SK, Christiansen SH, et al. Inflammatory cytokines break down intrinsic immunological tolerance of human primary keratinocytes to cytosolic DNA. J Immunol. 2014;192(5):2395–2404. doi: 10.4049/jimmunol.1302120
  30. Campanati A, Orciani M, Consales V, Lazzarini R, Ganzetti G, Di Benedetto G, et al. Characterization and profiling of immunomodulatory genes in resident mesenchymal stem cells reflect the Th1-Th17/Th2 imbalance of psoriasis. Arch Dermatol Res. 2014;306(10):915–920. doi: 10.1007/s00403-014-1493-3
  31. Wong K, Lew F, MacAry P, Kemeny D. CD40L-expressing CD8+ T cells prime CD8alpha+ DC for IL-12p70 production. Eur J Immunol. 2008;38:2251–2262. doi: 10.1002/eji.200838199
  32. Chong SZ, Wong KL, Lin G, Yang CM, Wong SC, Angeli V, et al. Human CD8+ T cells drive Th1 responses through the differentiation of TNF/iNOS-producing dendritic cells. Eur J Immunol. 2011;41(6):1639–1651. doi: 10.1002/eji.201041022.
  33. Fouser LA, Wright JF, Dunussi-Joannopoulos K, Collins M. Th17 cytokines and their emerging roles in inflammation and autoimmunity. Immunol Rev. 2008;226:87–102. doi: 10.1111/j.1600-065X.2008.00712.x
  34. Cargill M, Schrodi SJ, Chang M, Garcia VE, Brandon R, Callis KP, et al. A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet. 2007;80:273–290. doi: 10.1086/511051
  35. Ellinghaus E, Ellinghaus D, Stuart P, Nair RP, Debrus S, Raelson JV, et al. Genome-wide association study identifies a psoriasis susceptibility locus at TRAF3IP2. Nat Genet. 2010;42:991–995. doi: 10.1038/ng.689
  36. Tan JY, Li S, Yang K, Ma B, Chen W, Zha C, Zhang J, et al. Ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: a meta-analysis. J Dermatolog Treat. 2011;22(6):323–336. doi: 10.3109/09546634.2010.487890
  37. Gordon KB, Leonardi CL, Lebwohl M, Blauvelt A, Cameron GS, Braun D, et al. A 52-week, open-label study of the efficacy and safety of ixekizumab, an anti-interleukin-17A monoclonal antibody, in patients with chronic plaque psoriasis. J Am Acad Dermatol. 2014;71(6):1176–1182. doi: 10.1016/j.jaad.2014.07.048
  38. Mease PJ. Inhibition of interleukin-17, interleukin-23 and the TH17 cell pathway in the treatment of psoriatic arthritis and psoriasis. Curr Opin Rheumatol. 2015;27(2):127–133. doi: 10.1097/BOR.0000000000000147
  39. Acosta-Rodriguez EV, Rivino L, Geginat J, Jarrossay D, Gattorno M, Lanzavecchia A, et al. Surface phenotype and antigenic specificity of human interleukin 17-producing T helper memory cells. Nat Immunol 2007;8:639–646. doi: 10.1038/ni1467
  40. Cosmi L, De Palma R, Santarlasci V, Maggi L, Capone M, Frosali F, et al. Human interleukin-17-producing cells originate from a CD161+ CD4+ T cell precursor. J Exp Med 2008;205:1903–1916. doi: 10.1084/jem.20080397
  41. Maggi L, Santarlasci V, Capone M, Peired A, Frosali F, Crome SQ, et al. CD161 is a marker of all human IL-17-producing T-cell subsets and is induced by RORC. Eur J Immunol. 2010;40(8):2174–2181. doi: 10.1002/eji.200940257
  42. Miossec P, Kolls JK. Targeting IL-17 and TH17 cells in chronic inflammation. Nat Rev Drug Discov. 2012;11:763–776. doi: 10.1038/nrd3794
  43. Zhu S, Qian Y. IL-17/IL-17 receptor system in autoimmune disease: mechanisms and therapeutic potential. Clin Sci (Lond). 2012;122(11):487–511. doi: 10.1042/CS20110496
  44. Cosmi L, Liotta F, Maggi E, Romagnani S, Annunziato F. Th17 and non-classic Th1 cells in chronic inflammatory disorders: two sides of the same coin. Int Arch Allergy Immunol. 2014;164(3):171–177. doi: 10.1159/000363502
  45. Chan JR, Blumenschein W, Murphy E, Diveu C, Wiekowski M, Abbondanzo S, et al. IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med 2006;203:2577–2587. doi: 10.1084/jem.20060244
  46. Zhu S, Qian Y. IL-17/IL-17 receptor system in autoimmune disease: mechanisms and therapeutic potential. Clin Sci (Lond). 2012;122(11):487–511. doi: 10.1042/CS20110496
  47. Hsu HC, Yang P, Wang J, Wu Q, Myers R, Chen J, et al. Interleukin 17-producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice. Nat. Immunol. 2008;9:166–175. doi: 10.1038/ni1552
  48. Rangel-Moreno J, Carragher DM, Luz Garcia-Hernandez M, Hwang JY, Kusser K, Hartson L, et al. The development of inducible bronchus-associated lymphoid tissue depends on IL-17. Nature Immunology 2011;12:639–646. doi: 10.1038/ni.2053
  49. Rogers PR, Dubey C, Swain SL. Qualitative changes accompany memory T cell generation: faster, more effective responses at lower doses of antigen. J Immunol. 2000;164(5):2338–2346. doi: 10.4049/jimmunol.164.5.2338.
  50. Sallusto F, Geginat J, Lanzavecchia A. Central memory and effector memory T cell subsets: function, generation, and maintenance. Annu Rev Immunol. 2004;22:745–763. doi: 10.1146/annurev.immunol.22.012703.104702
  51. Clark RA. Resident memory T cells in human health and disease. Sci Transl Med. 2015;7(269):269rv1. doi: 10.1126/scitranslmed.3010641
  52. Padovan E. Modulation of CD4+ T Helper Cell Memory Responses in the Human Skin. Int Arch Allergy Immunol. 2017;173(3):121–137. doi: 10.1159/000477728
  53. McLachlan JB, Catron DM, Moon JJ, Jenkins MK. Dendritic cell antigen presentation drives simultaneous cytokine production by effector and regulatory T cells in inflamed skin. Immunity. 2009 Feb 20;30(2):277–288. doi: 10.1016/j.immuni.2008.11.013
  54. Elyaman W, KivisГ¤kk P, Reddy J, Chitnis T, Raddassi K, Imitola J, Bradshaw E, Kuchroo VK, Yagita H, Sayegh MH, Khoury SJ. Distinct functions of autoreactive memory and effector CD4+ T cells in experimental autoimmune encephalomyelitis. Am J Pathol. 2008 Aug;173(2):411–422. doi: 10.2353/ajpath.2008.080142
  55. Gaide O. Skin memory: the clinical implications. Rev Med Suisse. 2016;12(512):631–634.
  56. Mueller SN, Mackay LK. Tissue-resident memory T cells: local specialists in immune defence. Nat Rev Immunol. 2016;16:79–89. doi: 10.1038/nri.2015.3
  57. Zaid A, Hor JL, Christo SN, Groom JR, Heath WR, Mackay LK, et al. Chemokine Receptor–Dependent Control of Skin Tissue–Resident Memory T Cell Formation. J Immunol. 2017;199(7):2451–2459. doi: 10.4049/jimmunol.1700571
  58. Pan Y, Kupper TS. Metabolic Reprogramming and Longevity of Tissue-Resident Memory T Cells. Front Immunol. 2018;9:1347. doi: 10.3389/fimmu.2018.01347
  59. Cheuk S, Wikén M, Blomqvist L, Nylén S, Talme T, Ståhle M, et al. Epidermal Th22 and Tc17 cells form a localized disease memory in clinically healed psoriasis. J Immunol. 2014;192:3111. doi: 10.4049/jimmunol.1302313
  60. Gallais Sérézal I, Classon C, Cheuk S, Barrientos-Somarribas M, Wadman E, Martini E, et al. Resident T Cells in Resolved Psoriasis Steer Tissue Responses that Stratify Clinical Outcome. J Invest Dermatol. 2018;138(8):1754–1763. doi: 10.1016/j.jid.2018.02.030
  61. Kurihara K, Fujiyama T, Phadungsaksawasdi P, Ito T, Tokura Y. Significance of IL-17A-producing CD8+CD103+ skin resident memory T cells in psoriasis lesion and their possible relationship to clinical course. J Dermatol Sci. 2019;95(1):21–27. doi: 10.1016/j.jdermsci.2019.06.002
  62. Bhushan M, Bleiker TO, Ballsdon AE, Allen MH, Sopwith M, Robinson MK, et al. Anti-E-selectin is ineffective in the treatment of psoriasis: a randomized trial. Br J Dermatol. 2002;146(5):824–831. doi: 10.1046/j.1365-2133.2002.04743.x
  63. Boyman O, Hefti HP, Conrad C, Nickoloff BJ, Suter M, Nestle FO. Spontaneous development of psoriasis in a new animal model shows an essential role for resident T cells and tumor necrosis factor-α. J Exp Med. 2004;199:731–736. doi: 10.1084/jem.20031482
  64. Khairutdinov VR, Mikhailichenko AF, Belousova IE, Kuligina ES, Samtsov AV, Imyanitov EN. The role of intradermal proliferation of T-cells in the pathogenesis of psoriasis. An Bras Dermatol. 2017;92(1):41–44. doi: 10.1590/abd1806-4841.20175765
  65. Tarcha EJ, Olsen CM, Probst P, Peckham D, Muñoz-Elías EJ, Kruger JG, et al. Safety and pharmacodynamics of dalazatide, a Kv1.3 channel inhibitor, in the treatment of plaque psoriasis: A randomized phase 1b trial. PLoS One. 2017;12(7):e0180762. doi: 10.1371/journal.pone.0180762
  66. Bonefeld CM, Geisler C. The role of innate lymphoid cells in healthy and inflamed skin. Immunol Lett. 2016;179:25–28. doi: 10.1016/j.imlet.2016.01.005
  67. Xiong T, Turner JE. Innate lymphoid cells in autoimmunity and chronic inflammatory diseases. Semin Immunopathol. 2018;40(4):393–406. doi: 10.1007/s00281-018-0670-4
  68. Walker JA, Barlow JL, McKenzie AN. Innate lymphoid cells — how did we miss them? Nat Rev Immunol. 2013;13:75–87. doi: 10.1038/nri3349
  69. Teunissen MBM, Munneke JM, Bernink JH, Spuls PI, Res PCM, Te Velde A, et al. Composition of Innate Lymphoid Cell Subsets in the Human Skin: Enrichment of NCR(+) ILC3 in Lesional Skin and Blood of Psoriasis Patients. J Invest Dermatol. 2014;134(9):2351–2360. doi: 10.1038/jid.2014.146
  70. Spits H, Artis D, Colonna M. Innate lymphoid cells — a proposal for uniform nomenclature. Nat Rev Immunol. 2013;13(2):145–149. doi: 10.1038/nri3365
  71. Brüggen MC, Bauer WM, Reininger B, Clim E, Captarencu C, Steiner GE, et al. In Situ Mapping of Innate Lymphoid Cells in Human Skin: Evidence for Remarkable Differences between Normal and Inflamed Skin. J Invest Dermatol. 2016;136(12):2396–2405. doi: 10.1016/j.jid.2016.07.017
  72. Quaresma JAS. Organization of the Skin Immune System and Compartmentalized Immune Responses in Infectious Diseases. Clin Microbiol Rev. 2019;32(4):e00034-18. doi: 10.1128/CMR.00034-18
  73. Pantelyushin S, Haak S, Ingold B, Kulig P, Heppner FL, Navarini AA, et al. Rorγt+ innate lymphocytes and γδ T cells initiate psoriasiform plaque formation in mice. J Clin Invest. 2012;122(6):2252–2256. doi: 10.1172/JCI61862
  74. Dyring-Andersen B, Geisler C, Agerbeck C, Lauritsen JPH, Gúdjonsdottir SD, Skov L, et al. Increased number and frequency of group 3 innate lymphoid cells in nonlesional psoriatic skin. Br J Dermatol. 2014;170(3):609–616. oi: 10.1111/bjd.12658
  75. Villanova F, Flutter B, Tosi I, Grys K, Sreeneebus H, Perera GK, et al. Characterization of innate lymphoid cells in human skin and blood demonstrates increase of NKp44+ ILC3 in psoriasis. J Invest Dermatol. 2014;134:984–991. doi: 10.1038/jid.2013.477
  76. Keren A, Shemer A, Ginzburg A, Ullmann Y, Schrum AG, Paus R, et al. Innate lymphoid cells 3 induce psoriasis in xenotransplanted healthy human skin. J Allergy Clin Immunol. 2018;142(1):305–308. doi: 10.1016/j.jaci.2018.02.015
  77. Albanesi C, Scarponi C, Pallotta S, Daniele R, Bosisio D, Madonna S. Chemerin expression marks early psoriatic skin lesions and correlates with plasmacytoid dendritic cell recruitment. J Exp Med. 2009;206(1):249–58. doi: 10.1084/jem.20080129
  78. Berthier-Vergnes O, Bermond F, Flacher V, Massacrier C, Schmitt D, Peguet-Navarro J. TNF-alpha enhances phenotypic and functional maturation of humanepidermal Langerhans cells and induces IL-12 p40 and IP-10/CXCL-10 production. FEBS Lett. 2005;579(17):3660–3668. doi: 10.1016/j.febslet.2005.04.087
  79. Krueger JG, Bowcock A. Psoriasis pathophysiology: current concepts of pathogenesis. Ann Rheum Dis. 2005 Mar;64 Suppl 2 (Suppl 2):ii30-6. doi: 10.1136/ard.2004.031120
  80. Chong SZ, Wong KL, Lin G, Yang CM, Wong SC, Angeli V, Macary PA, Kemeny DM. Human CD8вЃє T cells drive Th1 responses through the differentiation of TNF/iNOS-producing dendritic cells. Eur J Immunol. 2011;41(6):1639–1651. doi: 10.1002/eji.201041022
  81. Wilsmann-Theis D, Koch S, Mindnich C, Bonness S, Schnautz S, von Bubnoff D, Bieber T. Generation and functional analysis of human TNF-О±/iNOS-producing dendritic cells (Tip-DC). Allergy. 2013l;68(7):890–898. doi: 10.1111/all.12172
  82. Lowes MA, Chamian F, Abello MV, Fuentes‐Duculan J, Lin SL, Nussbaum R, Novitskaya I, et al. Increase in TNF‐alpha and inducible nitric oxide synthase‐expressing dendritic cells in psoriasis and reduction with efalizumab (anti‐CD11a). Proc Natl Acad Sci U S A. 2005;102(52):19057–19062. doi: 10.1073/pnas.0509736102
  83. Wang CQF, Akalu YT, Suarez-Farinas M, Gonzalez J, Mitsui H, Lowes MA, Orlow SJ, Manga P, Krueger JG. IL-17 and TNF synergistically modulate cytokine expression while suppressing melanogenesis: potential relevance to psoriasis. JInvest Dermatol. 2013;133(12):2741–2752. doi: 10.1038/jid.2013.237
  84. Valdimarsson H, Thorleifsdottir RH, Sigurdardottir SL, Gudjonsson JE, Johnston A. Psoriasis — as an autoimmune disease caused by molecular mimicry. Trends Immunol. 2009; 30:494–501. doi: 10.1016/j.it.2009.07.008
  85. Thorleifsdottir RH, Sigurdardottir SL, Sigurgeirsson B, Olafsson JH, Sigurdsson MI, Petersen H, et al. Improvement of psoriasis after tonsillectomy is associated with a decrease in the frequency of circulating T cells that recognize streptococcal determinants and homologous skin determinants. J Immunol. 2012;188:5160–5165. doi: 10.4049/jimmunol.1102834
  86. Gudmundsdottir AS, Sigmundsdottir H, Sigurgeirsson B, Good MF, Valdimarsson H, Jonsdottir I. Is an epitope on keratin 17 a major target for autoreactive T lymphocytes in psoriasis? Clin Exp Immunol. 1999;117(3): 580–586. doi: 10.1046/j.1365-2249.1999.01013.x
  87. Baker BS, Laman JD, Powles A, van der Fits L, Voerman JS, Melief MJ, et al. Peptidoglycan and peptidoglycan-specific Th1 cells in psoriatic skin lesions. J Pathol. 2006;209(2):174–181. doi: 10.1002/path.1954
  88. Qian L, Chen W, Sun W, Li M, Zheng R, Qian Q, et al. Antimicrobial peptide LL-37 along with peptidoglycan drive monocyte polarization toward CD14(high)CD16(+) subset and may play a crucial role in the pathogenesis of psoriasis guttata. Am J Transl Res. 2015;7(6):1081–1094
  89. Baker BS, Powles A, Fry L. Peptidoglycan: a major aetiological factor for psoriasis? Trends in Immunology. 2006;27(12):545–551. doi: 10.1016/j.it.2006.10.001
  90. Flendrie M, Vissers WH, Creemers MC, de Jong EM, van de Kerkhof PC, van Riel PL. Dermatological conditions during TNF-alpha-blocking therapy in patients with rheumatoid arthritis: a prospective study. Arthritis Res Ther. 2005;7(3):R666-76. doi: 10.1186/ar1724
  91. Palucka AK, Blanck JP, Bennett L, Pascual V, Banchereau J. Cross-regulation of TNF and IFN-alpha in autoimmune diseases. Proc Natl Acad Sci U S A. 2005;102(9):3372–3377. doi: 10.1073/pnas.0408506102.
  92. Seneschal J, Milpied B, Vergier B, Lepreux S, Schaeverbeke T, Taïeb A. Cytokine imbalance with increased production of interferon-alpha in psoriasiform eruptions associated with antitumour necrosis factor-alpha treatments. Br J Dermatol. 2009;161(5):1081–1988. doi: 10.1111/j.1365-2133.2009.09329.x
  93. Chen X, Bäumel M, Männel DN, Howard OM, Oppenheim JJ. Interaction of TNF with TNF receptor type 2 promotes expansion and function of mouse CD4+CD25+ T regulatory cells. J Immunol. 2007;179(1):154–161. doi: 10.4049/jimmunol.179.1.154
  94. Ma HL, Napierata L, Stedman N, Benoit S, Collins M, Nickerson-Nutter C, Young DA. Tumor necrosis factor alpha blockade exacerbates murine psoriasis-like disease by enhancing Th17 function and decreasing expansion of Treg cells. Arthritis Rheum. 2010;62(2):430–440. doi: 10.1002/art.27203
  95. Collamer AN, Guerrero KT, Henning JS, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum. 2008;59(7):996–1001. doi: 10.1002/art.23835

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Согласие на обработку персональных данных с помощью сервиса «Яндекс.Метрика»

1. Я (далее – «Пользователь» или «Субъект персональных данных»), осуществляя использование сайта https://journals.rcsi.science/ (далее – «Сайт»), подтверждая свою полную дееспособность даю согласие на обработку персональных данных с использованием средств автоматизации Оператору - федеральному государственному бюджетному учреждению «Российский центр научной информации» (РЦНИ), далее – «Оператор», расположенному по адресу: 119991, г. Москва, Ленинский просп., д.32А, со следующими условиями.

2. Категории обрабатываемых данных: файлы «cookies» (куки-файлы). Файлы «cookie» – это небольшой текстовый файл, который веб-сервер может хранить в браузере Пользователя. Данные файлы веб-сервер загружает на устройство Пользователя при посещении им Сайта. При каждом следующем посещении Пользователем Сайта «cookie» файлы отправляются на Сайт Оператора. Данные файлы позволяют Сайту распознавать устройство Пользователя. Содержимое такого файла может как относиться, так и не относиться к персональным данным, в зависимости от того, содержит ли такой файл персональные данные или содержит обезличенные технические данные.

3. Цель обработки персональных данных: анализ пользовательской активности с помощью сервиса «Яндекс.Метрика».

4. Категории субъектов персональных данных: все Пользователи Сайта, которые дали согласие на обработку файлов «cookie».

5. Способы обработки: сбор, запись, систематизация, накопление, хранение, уточнение (обновление, изменение), извлечение, использование, передача (доступ, предоставление), блокирование, удаление, уничтожение персональных данных.

6. Срок обработки и хранения: до получения от Субъекта персональных данных требования о прекращении обработки/отзыва согласия.

7. Способ отзыва: заявление об отзыве в письменном виде путём его направления на адрес электронной почты Оператора: info@rcsi.science или путем письменного обращения по юридическому адресу: 119991, г. Москва, Ленинский просп., д.32А

8. Субъект персональных данных вправе запретить своему оборудованию прием этих данных или ограничить прием этих данных. При отказе от получения таких данных или при ограничении приема данных некоторые функции Сайта могут работать некорректно. Субъект персональных данных обязуется сам настроить свое оборудование таким способом, чтобы оно обеспечивало адекватный его желаниям режим работы и уровень защиты данных файлов «cookie», Оператор не предоставляет технологических и правовых консультаций на темы подобного характера.

9. Порядок уничтожения персональных данных при достижении цели их обработки или при наступлении иных законных оснований определяется Оператором в соответствии с законодательством Российской Федерации.

10. Я согласен/согласна квалифицировать в качестве своей простой электронной подписи под настоящим Согласием и под Политикой обработки персональных данных выполнение мною следующего действия на сайте: https://journals.rcsi.science/ нажатие мною на интерфейсе с текстом: «Сайт использует сервис «Яндекс.Метрика» (который использует файлы «cookie») на элемент с текстом «Принять и продолжить».