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Etanercept suppresses regenerative hyperplasia in psoriasis by acutely downregulating epidermal expression of interleukin (IL)‐19, IL‐20 and IL‐24

dc.contributor.authorWang, F.en_US
dc.contributor.authorSmith, N.en_US
dc.contributor.authorMaier, L.en_US
dc.contributor.authorXia, W.en_US
dc.contributor.authorHammerberg, C.en_US
dc.contributor.authorChubb, H.en_US
dc.contributor.authorChen, C.en_US
dc.contributor.authorRiblett, M.en_US
dc.contributor.authorJohnston, A.en_US
dc.contributor.authorGudjonsson, J.E.en_US
dc.contributor.authorHelfrich, Y.en_US
dc.contributor.authorKang, S.en_US
dc.contributor.authorFisher, G.J.en_US
dc.contributor.authorVoorhees, J.J.en_US
dc.date.accessioned2012-07-12T17:25:04Z
dc.date.available2013-09-03T15:38:27Zen_US
dc.date.issued2012-07en_US
dc.identifier.citationWang, F.; Smith, N.; Maier, L.; Xia, W.; Hammerberg, C.; Chubb, H.; Chen, C.; Riblett, M.; Johnston, A.; Gudjonsson, J.E.; Helfrich, Y.; Kang, S.; Fisher, G.J.; Voorhees, J.J. (2012). "Etanercept suppresses regenerative hyperplasia in psoriasis by acutely downregulating epidermal expression of interleukin (IL)‐19, IL‐20 and IL‐24." British Journal of Dermatology 167(1). <http://hdl.handle.net/2027.42/92088>en_US
dc.identifier.issn0007-0963en_US
dc.identifier.issn1365-2133en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/92088
dc.publisherBlackwell Publishing Ltden_US
dc.publisherWiley Periodicals, Inc.en_US
dc.titleEtanercept suppresses regenerative hyperplasia in psoriasis by acutely downregulating epidermal expression of interleukin (IL)‐19, IL‐20 and IL‐24en_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelDermatologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Dermatology, University of Michigan, Ann Arbor, MI 48109, U.S.A.en_US
dc.contributor.affiliationotherThe Johns Hopkins Department of Dermatology, Baltimore, MD, U.S.A.en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/92088/1/BJD_10961_sm_FigS2.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/92088/2/BJD_10961_sm_FigS3.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/92088/3/j.1365-2133.2012.10961.x.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/92088/4/BJD_10961_sm_FigS4.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/92088/5/BJD_10961_sm_FigS1.pdf
dc.identifier.doi10.1111/j.1365-2133.2012.10961.xen_US
dc.identifier.sourceBritish Journal of Dermatologyen_US
dc.identifier.citedreferenceMoore A, Gordon KB, Kang S et al. A randomized, open‐label trial of continuous versus interrupted etanercept therapy in the treatment of psoriasis. J Am Acad Dermatol 2007; 56: 598 – 603.en_US
dc.identifier.citedreferenceKunz S, Wolk K, Witte E et al. Interleukin (IL)‐19, IL‐20 and IL‐24 are produced by and act on keratinocytes and are distinct from classical ILs. Exp Dermatol 2006; 15: 991 – 1004.en_US
dc.identifier.citedreferenceTohyama M, Hanakawa Y, Shirakata Y et al. IL‐17 and IL‐22 mediate IL‐20 subfamily cytokine production in cultured keratinocytes via increased IL‐22 receptor expression. Eur J Immunol 2009; 39: 2779 – 88.en_US
dc.identifier.citedreferenceNagalakshmi ML, Murphy E, McClanahan T et al. Expression patterns of IL‐10 ligand and receptor gene families provide leads for biological characterization. Int Immunopharmacol 2004; 4: 577 – 92.en_US
dc.identifier.citedreferenceWolk K, Kunz S, Asadullah K et al. Cutting edge: immune cells as sources and targets of the IL‐10 family members? J Immunol 2002; 168: 5397 – 402.en_US
dc.identifier.citedreferenceWolk K, Witte K, Witte E et al. Maturing dendritic cells are an important source of IL‐29 and IL‐20 that may cooperatively increase the innate immunity of keratinocytes. J Leukoc Biol 2008; 83: 1181 – 93.en_US
dc.identifier.citedreferenceZaba LC, Cardinale I, Gilleaudeau P et al. Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses. J Exp Med 2007; 204: 3183 – 94.en_US
dc.identifier.citedreferenceParrish‐Novak J, Xu W, Brender T et al. Interleukins 19, 20, and 24 signal through two distinct receptor complexes. Differences in receptor–ligand interactions mediate unique biological functions. J Biol Chem 2002; 277: 47517 – 23.en_US
dc.identifier.citedreferenceWolk K, Haugen HS, Xu W et al. IL‐22 and IL‐20 are key mediators of the epidermal alterations in psoriasis while IL‐17 and IFN‐gamma are not. J Mol Med 2009; 87: 523 – 36.en_US
dc.identifier.citedreferenceStoler A, Kopan R, Duvic M et al. Use of monospecific antisera and cRNA probes to localize the major changes in keratin expression during normal and abnormal epidermal differentiation. J Cell Biol 1988; 107: 427 – 46.en_US
dc.identifier.citedreferenceMansbridge JN, Knapp AM, Strefling AM. Evidence for an alternative pathway of keratinocyte maturation in psoriasis from an antigen found in psoriatic but not normal epidermis. J Invest Dermatol 1984; 83: 296 – 301.en_US
dc.identifier.citedreferenceZaba LC, Suárez‐Fariñas M, Fuentes‐Duculan J et al. Effective treatment of psoriasis with etanercept is linked to suppression of IL‐17 signaling, not immediate response TNF genes. J Allergy Clin Immunol 2009; 124: 1022 – 10.en_US
dc.identifier.citedreferenceKang S, Cho S, Chung JH et al. Inflammation and extracellular matrix degradation mediated by activated transcription factors nuclear factor‐kappaB and activator protein‐1 in inflammatory acne lesions in vivo. Am J Pathol 2005; 166: 1691 – 9.en_US
dc.identifier.citedreferenceQuan T, Qin Z, Xia W et al. Matrix‐degrading metalloproteinases in photoaging. J Investig Dermatol Symp Proc 2009; 14: 20 – 4.en_US
dc.identifier.citedreferenceElder JT, Fisher GJ, Zhang QY et al. Retinoic acid receptor gene expression in human skin. J Invest Dermatol 1991; 96: 425 – 33.en_US
dc.identifier.citedreferenceLangley RG, Ellis CN. Evaluating psoriasis with Psoriasis Area and Severity Index, Psoriasis Global Assessment, and Lattice System Physician’s Global Assessment. J Am Acad Dermatol 2004; 51: 563 – 9.en_US
dc.identifier.citedreferenceOtkjaer K, Kragballe K, Funding AT et al. The dynamics of gene expression of interleukin‐19 and interleukin‐20 and their receptors in psoriasis. Br J Dermatol 2005; 153: 911 – 18.en_US
dc.identifier.citedreferenceBlumberg H, Conklin D, Xu WF et al. Interleukin 20: discovery, receptor identification, and role in epidermal function. Cell 2001; 104: 9 – 19.en_US
dc.identifier.citedreferenceDumoutier L, Leemans C, Lejeune D et al. Cutting edge: STAT activation by IL‐19, IL‐20 and mda‐7 through IL‐20 receptor complexes of two types. J Immunol 2001; 167: 3545 – 9.en_US
dc.identifier.citedreferenceBaker BS, Swain AF, Fry L et al. Epidermal T lymphocytes and HLA‐DR expression in psoriasis. Br J Dermatol 1984; 110: 555 – 64.en_US
dc.identifier.citedreferenceBos JD, Hulsebosch HJ, Krieg SR et al. Immunocompetent cells in psoriasis. In situ immunophenotyping by monoclonal antibodies. Arch Dermatol Res 1983; 275: 181 – 9.en_US
dc.identifier.citedreferenceKrueger JG. The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol 2002; 46: 1 – 23.en_US
dc.identifier.citedreferenceBhagavathula N, Nerusu KC, Fisher GJ et al. Amphiregulin and epidermal hyperplasia: amphiregulin is required to maintain the psoriatic phenotype of human skin grafts on severe combined immunodeficient mice. Am J Pathol 2005; 166: 1009 – 16.en_US
dc.identifier.citedreferencePiepkorn M, Predd H, Underwood R et al. Proliferation–differentiation relationships in the expression of heparin‐binding epidermal growth factor‐related factors and erbB receptors by normal and psoriatic human keratinocytes. Arch Dermatol Res 2003; 295: 93 – 101.en_US
dc.identifier.citedreferenceChiricozzi A, Guttman‐Yassky E, Suárez‐Fariñas M et al. Integrative responses to IL‐17 and TNF‐α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis. J Invest Dermatol 2011; 131: 677 – 87.en_US
dc.identifier.citedreferenceHaider AS, Cohen J, Fei J et al. Insights into gene modulation by therapeutic TNF and IFNgamma antibodies: TNF regulates IFNgamma production by T cells and TNF‐regulated genes linked to psoriasis transcriptome. J Invest Dermatol 2008; 128: 655 – 66.en_US
dc.identifier.citedreferenceLee E, Trepicchio WL, Oestreicher JL et al. Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris. J Exp Med 2004; 199: 125 – 30.en_US
dc.identifier.citedreferenceGuilloteau K, Paris I, Pedretti N et al. Skin inflammation induced by the synergistic action of IL‐17A, IL‐22, oncostatin M, IL‐1α, and TNF‐α recapitulates some features of psoriasis. J Immunol 2010; 184: 5263 – 70.en_US
dc.identifier.citedreferenceSchroder JM, Harder J. Human beta‐defensin‐2. Int J Biochem Cell Biol 1999; 31: 645 – 51.en_US
dc.identifier.citedreferenceLowes MA, Bowcock AM, Krueger JG. Pathogenesis and therapy of psoriasis. Nature 2007; 445: 866 – 73.en_US
dc.identifier.citedreferenceClark RA. Skin‐resident T cells: the ups and downs of on site immunity. J Invest Dermatol 2010; 130: 362 – 70.en_US
dc.identifier.citedreferenceJohnson‐Huang LM, McNutt NS, Krueger JG et al. Cytokine‐producing dendritic cells in the pathogenesis of inflammatory skin diseases. J Clin Immunol 2009; 29: 247 – 56.en_US
dc.identifier.citedreferenceZaba LC, Krueger JG, Lowes MA. Resident and ‘inflammatory’ dendritic cells in human skin. J Invest Dermatol 2009; 129: 302 – 8.en_US
dc.identifier.citedreferenceNestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med 2009; 361: 496 – 509.en_US
dc.identifier.citedreferenceCiric B, El‐Behi M, Cabrera R et al. IL‐23 drives pathogenic IL‐17‐producing CD8+ T cells. J Immunol 2009; 182: 5296 – 305.en_US
dc.identifier.citedreferenceDuhen T, Geiger R, Jarrossay D et al. Production of interleukin 22 but not interleukin 17 by a subset of human skin‐homing memory T cells. Nat Immunol 2009; 10: 857 – 63.en_US
dc.identifier.citedreferenceSonnenberg GF, Fouser LA, Artis D. Border patrol: regulation of immunity, inflammation and tissue homeostasis at barrier surfaces by IL‐22. Nat Immunol 2011; 12: 383 – 90.en_US
dc.identifier.citedreferenceLiang SC, Tan XY, Luxenberg DP et al. Interleukin (IL)‐22 and IL‐17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides. J Exp Med 2006; 203: 2271 – 9.en_US
dc.identifier.citedreferenceNograles KE, Zaba LC, Guttman‐Yassky E et al. Th17 cytokines interleukin (IL)‐17 and IL‐22 modulate distinct inflammatory and keratinocyte‐response pathways. Br J Dermatol 2008; 159: 1092 – 102.en_US
dc.identifier.citedreferenceHarper EG, Guo C, Rizzo H et al. Th17 cytokines stimulate CCL20 expression in keratinocytes in vitro and in vivo: implications for psoriasis pathogenesis. J Invest Dermatol 2009; 129: 2175 – 83.en_US
dc.identifier.citedreferenceWolk K, Kunz S, Witte E et al. IL‐22 increases the innate immunity of tissues. Immunity 2004; 21: 241 – 54.en_US
dc.identifier.citedreferenceBoniface K, Bernard FX, Garcia M et al. IL‐22 inhibits epidermal differentiation and induces proinflammatory gene expression and migration of human keratinocytes. J Immunol 2005; 174: 3695 – 702.en_US
dc.identifier.citedreferenceZheng Y, Danilenko DM, Valdez P et al. Interleukin‐22, a T(H)17 cytokine, mediates IL‐23‐induced dermal inflammation and acanthosis. Nature 2007; 445: 648 – 51.en_US
dc.identifier.citedreferenceSa SM, Valdez PA, Wu J et al. The effects of IL‐20 subfamily cytokines on reconstituted human epidermis suggest potential roles in cutaneous innate defense and pathogenic adaptive immunity in psoriasis. J Immunol 2007; 178: 2229 – 40.en_US
dc.identifier.citedreferenceRes PC, Piskin G, de Boer OJ et al. Overrepresentation of IL‐17A and IL‐22 producing CD8 T cells in lesional skin suggests their involvement in the pathogenesis of psoriasis. PLoS ONE 2010; 5: e14108.en_US
dc.identifier.citedreferenceRomer J, Hasselager E, Norby PL et al. Epidermal overexpression of interleukin‐19 and ‐20 mRNA in psoriatic skin disappears after short‐term treatment with cyclosporine A or calcipotriol. J Invest Dermatol 2003; 121: 1306 – 11.en_US
dc.identifier.citedreferenceWang F, Lee E, Lowes MA et al. Prominent production of IL‐20 by CD68+/CD11c+ myeloid‐derived cells in psoriasis: gene regulation and cellular effects. J Invest Dermatol 2006; 126: 1590 – 9.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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