Evidence that a neutrophil-keratinocyte crosstalk is an early target of IL-17A inhibition in psoriasis
The response of psoriasis to antibodies targeting the interleukin (IL)‐23/IL‐17A pathway suggests a prominent role of T‐helper type‐17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate‐to‐severe psoriasis receiving 3 different in...
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| Published in | Experimental dermatology Vol. 24; no. 7; pp. 529 - 535 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Denmark
Blackwell Publishing Ltd
01.07.2015
John Wiley & Sons, Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0906-6705 1600-0625 1600-0625 |
| DOI | 10.1111/exd.12710 |
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| Abstract | The response of psoriasis to antibodies targeting the interleukin (IL)‐23/IL‐17A pathway suggests a prominent role of T‐helper type‐17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate‐to‐severe psoriasis receiving 3 different intravenous dosing regimens of the anti‐IL‐17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL‐17 and may store the cytokine preformed, as IL‐17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL‐17‐inducible neutrophil chemoattractants (e.g. CXCL1, CXCL8); effects on numbers of T cells and CD11c‐positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest‐dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil–keratinocyte axis in psoriasis that may involve neutrophil‐derived IL‐17 and is an early target of IL‐17A‐directed therapies such as secukinumab. |
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| AbstractList | The response of psoriasis to antibodies targeting the interleukin (IL)-23/IL-17A pathway suggests a prominent role of T-helper type-17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate-to-severe psoriasis receiving 3 different intravenous dosing regimens of the anti-IL-17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL-17 and may store the cytokine preformed, as IL-17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL-17-inducible neutrophil chemoattractants (e.g.
CXCL1
,
CXCL8
); effects on numbers of T cells and CD11c-positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest-dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil–keratinocyte axis in psoriasis that may involve neutrophil-derived IL-17 and is an early target of IL-17A-directed therapies such as secukinumab. The response of psoriasis to antibodies targeting the interleukin ( IL )‐23/ IL ‐17A pathway suggests a prominent role of T‐helper type‐17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate‐to‐severe psoriasis receiving 3 different intravenous dosing regimens of the anti‐ IL ‐17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL ‐17 and may store the cytokine preformed, as IL ‐17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL ‐17‐inducible neutrophil chemoattractants (e.g. CXCL 1 , CXCL 8 ); effects on numbers of T cells and CD 11c‐positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest‐dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil–keratinocyte axis in psoriasis that may involve neutrophil‐derived IL ‐17 and is an early target of IL ‐17A‐directed therapies such as secukinumab. The response of psoriasis to antibodies targeting the interleukin (IL)-23/IL-17A pathway suggests a prominent role of T-helper type-17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate-to-severe psoriasis receiving 3 different intravenous dosing regimens of the anti-IL-17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL-17 and may store the cytokine preformed, as IL-17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL-17-inducible neutrophil chemoattractants (e.g. CXCL1, CXCL8); effects on numbers of T cells and CD11c-positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest-dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil-keratinocyte axis in psoriasis that may involve neutrophil-derived IL-17 and is an early target of IL-17A-directed therapies such as secukinumab. The response of psoriasis to antibodies targeting the interleukin (IL)-23/IL-17A pathway suggests a prominent role of T-helper type-17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate-to-severe psoriasis receiving 3 different intravenous dosing regimens of the anti-IL-17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL-17 and may store the cytokine preformed, as IL-17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL-17-inducible neutrophil chemoattractants (e.g. CXCL1, CXCL8); effects on numbers of T cells and CD11c-positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest-dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil-keratinocyte axis in psoriasis that may involve neutrophil-derived IL-17 and is an early target of IL-17A-directed therapies such as secukinumab.The response of psoriasis to antibodies targeting the interleukin (IL)-23/IL-17A pathway suggests a prominent role of T-helper type-17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate-to-severe psoriasis receiving 3 different intravenous dosing regimens of the anti-IL-17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL-17 and may store the cytokine preformed, as IL-17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL-17-inducible neutrophil chemoattractants (e.g. CXCL1, CXCL8); effects on numbers of T cells and CD11c-positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest-dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil-keratinocyte axis in psoriasis that may involve neutrophil-derived IL-17 and is an early target of IL-17A-directed therapies such as secukinumab. The response of psoriasis to antibodies targeting the interleukin (IL)-23/IL-17A pathway suggests a prominent role of T-helper type-17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate-to-severe psoriasis receiving 3 different intravenous dosing regimens of the anti-IL-17A antibody secukinumab (1 3 mg/kg or 1 10 mg/kg on Day 1, or 3 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL-17 and may store the cytokine preformed, as IL-17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL-17-inducible neutrophil chemoattractants (e.g. CXCL1, CXCL8); effects on numbers of T cells and CD11c-positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest-dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil-keratinocyte axis in psoriasis that may involve neutrophil-derived IL-17 and is an early target of IL-17A-directed therapies such as secukinumab. The response of psoriasis to antibodies targeting the interleukin (IL)‐23/IL‐17A pathway suggests a prominent role of T‐helper type‐17 (Th17) cells in this disease. We examined the clinical and immunological response patterns of 100 subjects with moderate‐to‐severe psoriasis receiving 3 different intravenous dosing regimens of the anti‐IL‐17A antibody secukinumab (1 × 3 mg/kg or 1 × 10 mg/kg on Day 1, or 3 × 10 mg/kg on Days 1, 15 and 29) or placebo in a phase 2 trial. Baseline biopsies revealed typical features of active psoriasis, including epidermal accumulation of neutrophils and formation of microabscesses in >60% of cases. Neutrophils were the numerically largest fraction of infiltrating cells containing IL‐17 and may store the cytokine preformed, as IL‐17A mRNA was not detectable in neutrophils isolated from active plaques. Significant clinical responses to secukinumab were observed 2 weeks after a single infusion, associated with extensive clearance of cutaneous neutrophils parallel to the normalization of keratinocyte abnormalities and reduction of IL‐17‐inducible neutrophil chemoattractants (e.g. CXCL1, CXCL8); effects on numbers of T cells and CD11c‐positive dendritic cells were more delayed. Histological and immunological improvements were generally dose dependent and not observed in the placebo group. In the lowest‐dose group, a recurrence of neutrophils was seen in some subjects at Week 12; these subjects relapsed faster than those without microabscesses. Our findings are indicative of a neutrophil–keratinocyte axis in psoriasis that may involve neutrophil‐derived IL‐17 and is an early target of IL‐17A‐directed therapies such as secukinumab. |
| Author | Kolbinger, Frank Tu, John H. Bourcier, Marc Stingl, Georg Salter, Janeen M. Reich, Kristian Lee, David M. Kunynetz, Rodion A. Schumacher, Martin M. Wieczorek, Grazyna A. Papp, Kim A. Gratton, David Bleul, Conrad C. Kriehuber, Ernst Peters, Thomas Matheson, Robert T. Falk, Thomas M. Hueber, Wolfgang Rosoph, Les A. Sommer, Ulrike Bauer, Wolfgang M. Bissonnette, Robert Poulin, Yves Blödorn-Schlicht, Norbert A. |
| Author_xml | – sequence: 1 givenname: Kristian surname: Reich fullname: Reich, Kristian email: kreich@dermatologikum.de organization: Dermatologikum Hamburg and SCIderm Research Institute, Hamburg, Germany – sequence: 2 givenname: Kim A. surname: Papp fullname: Papp, Kim A. organization: Probity Medical Research Inc, ON, Waterloo, Canada – sequence: 3 givenname: Robert T. surname: Matheson fullname: Matheson, Robert T. organization: Oregon Medical Research Center PC, OR, Portland, USA – sequence: 4 givenname: John H. surname: Tu fullname: Tu, John H. organization: Skin Search of Rochester, RochesterNY, USA – sequence: 5 givenname: Robert surname: Bissonnette fullname: Bissonnette, Robert organization: Innovaderm Research Inc, QC, Montreal, Canada – sequence: 6 givenname: Marc surname: Bourcier fullname: Bourcier, Marc organization: Dermatology Clinic, NB, Moncton, Canada – sequence: 7 givenname: David surname: Gratton fullname: Gratton, David organization: International Dermatology Research, QC, Montreal, Canada – sequence: 8 givenname: Rodion A. surname: Kunynetz fullname: Kunynetz, Rodion A. organization: Ultranova Skincare, ON, Barrie, Canada – sequence: 9 givenname: Yves surname: Poulin fullname: Poulin, Yves organization: Centre de Recherche Dermatologique du Québec Métropolitain, QC, Quebec City, Canada – sequence: 10 givenname: Les A. surname: Rosoph fullname: Rosoph, Les A. organization: North Bay Dermatology Centre, ON, North Bay, Canada – sequence: 11 givenname: Georg surname: Stingl fullname: Stingl, Georg organization: Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, Medical University of Vienna, Vienna, Austria – sequence: 12 givenname: Wolfgang M. surname: Bauer fullname: Bauer, Wolfgang M. organization: Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, Medical University of Vienna, Vienna, Austria – sequence: 13 givenname: Janeen M. surname: Salter fullname: Salter, Janeen M. organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 14 givenname: Thomas M. surname: Falk fullname: Falk, Thomas M. organization: Dermatologikum Hamburg and SCIderm Research Institute, Hamburg, Germany – sequence: 15 givenname: Norbert A. surname: Blödorn-Schlicht fullname: Blödorn-Schlicht, Norbert A. organization: Dermatologikum Hamburg and SCIderm Research Institute, Hamburg, Germany – sequence: 16 givenname: Wolfgang surname: Hueber fullname: Hueber, Wolfgang organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 17 givenname: Ulrike surname: Sommer fullname: Sommer, Ulrike organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 18 givenname: Martin M. surname: Schumacher fullname: Schumacher, Martin M. organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 19 givenname: Thomas surname: Peters fullname: Peters, Thomas organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 20 givenname: Ernst surname: Kriehuber fullname: Kriehuber, Ernst organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 21 givenname: David M. surname: Lee fullname: Lee, David M. organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 22 givenname: Grazyna A. surname: Wieczorek fullname: Wieczorek, Grazyna A. organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 23 givenname: Frank surname: Kolbinger fullname: Kolbinger, Frank organization: Novartis Institutes for BioMedical Research, Basel, Switzerland – sequence: 24 givenname: Conrad C. surname: Bleul fullname: Bleul, Conrad C. organization: Novartis Institutes for BioMedical Research, Basel, Switzerland |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25828362$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1038/ni.2797 10.1111/bjd.12236 10.1084/jem.20071094 10.1111/j.1600-6143.2011.03867.x 10.1182/blood.V98.12.3309 10.1016/j.it.2012.11.005 10.1038/nrd3794 10.4049/jimmunol.181.1.669 10.1056/NEJMra0804595 10.1038/jid.2010.432 10.1111/bjd.12112 10.1111/imm.12142 10.1016/j.bbrc.2013.03.024 10.1111/bjd.12110 10.1038/jid.2013.526 10.1111/j.1744-9987.2012.01109.x 10.4049/jimmunol.1200385 10.1056/NEJMoa1109017 10.1111/j.1365-2133.2008.08769.x 10.1126/scitranslmed.3001107 10.1016/j.jaci.2012.04.024 10.1002/jlb.66.6.989 10.1371/journal.pone.0014108 10.4049/jimmunol.1100123 10.1111/j.1601-0825.2010.01704.x 10.1056/NEJMoa1109997 10.1056/NEJMoa1314258 10.1111/j.1365-2133.2008.08902.x 10.1084/jem.20132413 10.1016/S0140-6736(08)60726-6 10.1038/jid.2010.340 |
| ContentType | Journal Article |
| Copyright | 2015 The Authors. Published by John Wiley & Sons Ltd. 2015 The Authors. Experimental Dermatology Published by John Wiley & Sons Ltd. 2015 The Authors. Published by John Wiley & Sons Ltd. 2015 |
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| Keywords | IL-17A neutrophils psoriasis secukinumab |
| Language | English |
| License | Attribution http://creativecommons.org/licenses/by/4.0 2015 The Authors. Experimental Dermatology Published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Notes | Celgene Amgen GlaxoSmithKline Eli Lilly Tribute Merck Kyowa-Kirin istex:C283AA571BE4CE7B7ED00E45DBE40F5071E01FDC Lilly MSD Biogen-Idec Janssen-Cilag Medac Takeda and Vertex Pfizer ArticleID:EXD12710 Figure S1. Subject disposition. Figure S2. Images depicting semi-quantitative assessment categories. Figure S3. Study design. Figure S4. Assessment of peripheral blood T-lymphocyte subsets. Figure S5. Examples of control stainings in immunohistochemistry and immunofluorescence. Figure S6. Assessment of additional epidermal and cellular markers over time. Figure S7. Proposed simplified model of psoriasis pathogenesis and early effects of anti-IL-17 therapy. Table S1. NanoString nCounter Gene Expression Maestro CodeSet probe sequences for genes reported in this study. Table S2. Demographic and Baseline clinical characteristics of study subjects. AbbVie Fujisawa Forward Pharma Covagen Novartis Centocor ark:/67375/WNG-8Z7SPCDV-V Leo Astellas Novartis Pharma AG, Basel, Switzerland ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Undefined-3 Currently employed by Firalis SAS, Huningue, France. |
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| PublicationTitle | Experimental dermatology |
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| Publisher | Blackwell Publishing Ltd John Wiley & Sons, Ltd |
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| References | Keijsers R R, Hendriks A G, van Erp P E et al. J Invest Dermatol 2014: 134: 1276-1284. Johansen C, Usher P A, Kjellerup R B et al. Br J Dermatol 2009: 160: 319-324. Krueger J G, Fretzin S, Suárez-Fariñas M et al. J Allergy Clin Immunol 2012: 130: 145-154.e9. Keijsers R R, van der Velden H M, van Erp P E et al. Br J Dermatol 2013: 168: 1294-1302. Lowes M A, Russell C B, Martin D A et al. Trends Immunol 2013: 34: 174-181. Griffin G K, Newton G, Tarrio M L et al. J Immunol 2012: 188: 6287-6299. Forlow S B, Schurr J R, Kolls J K et al. Blood 2001: 98: 3309-3314. Miossec P, Kolls J K. Nat Rev Drug Discov 2012: 11: 763-776. Nestle F O, Kaplan D H, Barker J. N Engl J Med 2009: 361: 496-509. Papp K A, Langley R G, Lebwohl M et al. Lancet 2008: 371: 1675-1684. Zaba L C, Cardinale I, Gilleaudeau P et al. J Exp Med 2007: 204: 3183-3194. Taylor P R, Roy S, Leal S M Jr et al. Nat Immunol 2014: 15: 143-151. Cowland J B, Borregaard N. J Leukoc Biol 1999: 66: 989-995. Finsterbusch M, Voisin M B, Beyrau M et al. J Exp Med 2014: 11: 1307-1314. Hueber W, Patel D D, Dryja T et al. Sci Transl Med 2010: 2: 52ra72. Rich P, Sigurgeirsson B, Thaci D et al. Br J Dermatol 2013: 168: 402-411. Chiricozzi A, Guttman-Yassky E, Suárez-Fariñas M et al. J Invest Dermatol 2011: 131: 677-687. Res P C, Piskin G, de Boer O J et al. PLoS ONE 2010: 5: e14108. Lin A M, Rubin C J, Khandpur R et al. J Immunol 2011: 187: 490-500. Langley R G, Elewski B E, Lebwohl M et al.; ERASURE Study Group; FIXTURE Study Group. N Engl J Med 2014: 371: 326-338. Papp K A, Langley R G, Sigurgeirsson B et al. Br J Dermatol 2013: 168: 412-421. Skov L, Beurskens F J, Zachariae C O et al. J Immunol 2008: 181: 669-679. Nograles K E, Zaba L C, Guttman-Yassky E et al. Br J Dermatol 2008: 159: 1092-1102. Leonardi C, Matheson R, Zachariae C et al. N Engl J Med 2012: 366: 1190-1199. Yapici Ü, Roelofs J J, Florquin S. Am J Transplant 2012: 12: 504-505. Suzuki A, Haruna K, Mizuno Y et al. Ther Apher Dial 2012: 16: 445-448. Papp K A, Leonardi C, Menter A et al. N Engl J Med 2012: 366: 1181-1189. Kirkham B W, Kavanaugh A, Reich K. Immunology 2014: 141: 133-142. Türkoğlu O, Kandiloğlu G, Berdeli A et al. Oral Dis 2011: 17: 60-67. Lindroos J, Svensson L, Norsgaard H et al. J Invest Dermatol 2011: 131: 1110-1118. Chen X, Takai T, Xie Y et al. Biochem Biophys Res Commun 2011: 433: 532-537. 2011; 433 2012; 188 2007; 204 2012; 366 2009; 160 1999; 66 2013; 168 2014; 371 2012; 16 2011; 17 2012; 12 2012; 11 2014; 134 2011; 131 2008; 181 2012; 130 2013; 34 2014; 15 2008; 159 2009; 361 2010; 2 2010; 5 2014; 141 2008; 371 2014; 11 2011; 187 2001; 98 e_1_2_10_23_1 e_1_2_10_24_1 e_1_2_10_21_1 e_1_2_10_22_1 e_1_2_10_20_1 e_1_2_10_2_1 e_1_2_10_4_1 e_1_2_10_18_1 e_1_2_10_3_1 e_1_2_10_19_1 e_1_2_10_6_1 e_1_2_10_16_1 e_1_2_10_5_1 e_1_2_10_17_1 e_1_2_10_8_1 e_1_2_10_14_1 e_1_2_10_7_1 e_1_2_10_15_1 e_1_2_10_12_1 e_1_2_10_9_1 e_1_2_10_13_1 e_1_2_10_10_1 e_1_2_10_11_1 e_1_2_10_32_1 e_1_2_10_31_1 e_1_2_10_30_1 e_1_2_10_29_1 e_1_2_10_27_1 e_1_2_10_28_1 e_1_2_10_25_1 e_1_2_10_26_1 19641206 - N Engl J Med. 2009 Jul 30;361(5):496-509 23362969 - Br J Dermatol. 2013 Feb;168(2):402-11 22151104 - Am J Transplant. 2012 Feb;12(2):504-5; author reply 506 22566565 - J Immunol. 2012 Jun 15;188(12):6287-99 23291100 - Trends Immunol. 2013 Apr;34(4):174-81 23524263 - Biochem Biophys Res Commun. 2013 Apr 19;433(4):532-7 23330679 - Br J Dermatol. 2013 Jun;168(6):1294-302 18684158 - Br J Dermatol. 2008 Nov;159(5):1092-102 10614782 - J Leukoc Biol. 1999 Dec;66(6):989-95 21606249 - J Immunol. 2011 Jul 1;187(1):490-500 22455412 - N Engl J Med. 2012 Mar 29;366(13):1181-9 23106107 - Br J Dermatol. 2013 Feb;168(2):412-21 22455413 - N Engl J Med. 2012 Mar 29;366(13):1190-9 20926833 - Sci Transl Med. 2010 Oct 6;2(52):52ra72 19016708 - Br J Dermatol. 2009 Feb;160(2):319-24 23023676 - Nat Rev Drug Discov. 2012 Oct;11(10):763-76 24913232 - J Exp Med. 2014 Jun 30;211(7):1307-14 21289639 - J Invest Dermatol. 2011 May;131(5):1110-8 11719368 - Blood. 2001 Dec 1;98(12):3309-14 22677045 - J Allergy Clin Immunol. 2012 Jul;130(1):145-54.e9 18039949 - J Exp Med. 2007 Dec 24;204(13):3183-94 24317395 - J Invest Dermatol. 2014 May;134(5):1276-84 21085185 - J Invest Dermatol. 2011 Mar;131(3):677-87 25007392 - N Engl J Med. 2014 Jul 24;371(4):326-38 23819583 - Immunology. 2014 Feb;141(2):133-42 23046369 - Ther Apher Dial. 2012 Oct;16(5):445-8 18566434 - J Immunol. 2008 Jul 1;181(1):669-79 18486740 - Lancet. 2008 May 17;371(9625):1675-84 21124836 - PLoS One. 2010;5(11):e14108 24362892 - Nat Immunol. 2014 Feb;15(2):143-51 20646232 - Oral Dis. 2011 Jan;17(1):60-7 |
| References_xml | – reference: Lowes M A, Russell C B, Martin D A et al. Trends Immunol 2013: 34: 174-181. – reference: Türkoğlu O, Kandiloğlu G, Berdeli A et al. Oral Dis 2011: 17: 60-67. – reference: Chen X, Takai T, Xie Y et al. Biochem Biophys Res Commun 2011: 433: 532-537. – reference: Lin A M, Rubin C J, Khandpur R et al. J Immunol 2011: 187: 490-500. – reference: Chiricozzi A, Guttman-Yassky E, Suárez-Fariñas M et al. J Invest Dermatol 2011: 131: 677-687. – reference: Papp K A, Langley R G, Lebwohl M et al. Lancet 2008: 371: 1675-1684. – reference: Leonardi C, Matheson R, Zachariae C et al. N Engl J Med 2012: 366: 1190-1199. – reference: Papp K A, Leonardi C, Menter A et al. N Engl J Med 2012: 366: 1181-1189. – reference: Miossec P, Kolls J K. Nat Rev Drug Discov 2012: 11: 763-776. – reference: Hueber W, Patel D D, Dryja T et al. Sci Transl Med 2010: 2: 52ra72. – reference: Griffin G K, Newton G, Tarrio M L et al. J Immunol 2012: 188: 6287-6299. – reference: Skov L, Beurskens F J, Zachariae C O et al. J Immunol 2008: 181: 669-679. – reference: Yapici Ü, Roelofs J J, Florquin S. Am J Transplant 2012: 12: 504-505. – reference: Lindroos J, Svensson L, Norsgaard H et al. J Invest Dermatol 2011: 131: 1110-1118. – reference: Taylor P R, Roy S, Leal S M Jr et al. Nat Immunol 2014: 15: 143-151. – reference: Krueger J G, Fretzin S, Suárez-Fariñas M et al. J Allergy Clin Immunol 2012: 130: 145-154.e9. – reference: Cowland J B, Borregaard N. J Leukoc Biol 1999: 66: 989-995. – reference: Keijsers R R, Hendriks A G, van Erp P E et al. J Invest Dermatol 2014: 134: 1276-1284. – reference: Keijsers R R, van der Velden H M, van Erp P E et al. Br J Dermatol 2013: 168: 1294-1302. – reference: Suzuki A, Haruna K, Mizuno Y et al. Ther Apher Dial 2012: 16: 445-448. – reference: Nestle F O, Kaplan D H, Barker J. N Engl J Med 2009: 361: 496-509. – reference: Forlow S B, Schurr J R, Kolls J K et al. Blood 2001: 98: 3309-3314. – reference: Nograles K E, Zaba L C, Guttman-Yassky E et al. Br J Dermatol 2008: 159: 1092-1102. – reference: Kirkham B W, Kavanaugh A, Reich K. Immunology 2014: 141: 133-142. – reference: Langley R G, Elewski B E, Lebwohl M et al.; ERASURE Study Group; FIXTURE Study Group. N Engl J Med 2014: 371: 326-338. – reference: Finsterbusch M, Voisin M B, Beyrau M et al. J Exp Med 2014: 11: 1307-1314. – reference: Res P C, Piskin G, de Boer O J et al. PLoS ONE 2010: 5: e14108. – reference: Zaba L C, Cardinale I, Gilleaudeau P et al. J Exp Med 2007: 204: 3183-3194. – reference: Papp K A, Langley R G, Sigurgeirsson B et al. Br J Dermatol 2013: 168: 412-421. – reference: Johansen C, Usher P A, Kjellerup R B et al. Br J Dermatol 2009: 160: 319-324. – reference: Rich P, Sigurgeirsson B, Thaci D et al. Br J Dermatol 2013: 168: 402-411. – volume: 130 start-page: 145 year: 2012 end-page: 154 publication-title: J Allergy Clin Immunol – volume: 187 start-page: 490 year: 2011 end-page: 500 publication-title: J Immunol – volume: 188 start-page: 6287 year: 2012 end-page: 6299 publication-title: J Immunol – volume: 17 start-page: 60 year: 2011 end-page: 67 publication-title: Oral Dis – volume: 12 start-page: 504 year: 2012 end-page: 505 publication-title: Am J Transplant – volume: 159 start-page: 1092 year: 2008 end-page: 1102 publication-title: Br J Dermatol – volume: 134 start-page: 1276 year: 2014 end-page: 1284 publication-title: J Invest Dermatol – volume: 131 start-page: 1110 year: 2011 end-page: 1118 publication-title: J Invest Dermatol – volume: 16 start-page: 445 year: 2012 end-page: 448 publication-title: Ther Apher Dial – volume: 15 start-page: 143 year: 2014 end-page: 151 publication-title: Nat Immunol – volume: 11 start-page: 1307 year: 2014 end-page: 1314 publication-title: J Exp Med – volume: 131 start-page: 677 year: 2011 end-page: 687 publication-title: J Invest Dermatol – volume: 361 start-page: 496 year: 2009 end-page: 509 publication-title: N Engl J Med – volume: 160 start-page: 319 year: 2009 end-page: 324 publication-title: Br J Dermatol – volume: 34 start-page: 174 year: 2013 end-page: 181 publication-title: Trends Immunol – volume: 168 start-page: 402 year: 2013 end-page: 411 publication-title: Br J Dermatol – volume: 98 start-page: 3309 year: 2001 end-page: 3314 publication-title: Blood – volume: 371 start-page: 326 year: 2014 end-page: 338 publication-title: N Engl J Med – volume: 66 start-page: 989 year: 1999 end-page: 995 publication-title: J Leukoc Biol – volume: 204 start-page: 3183 year: 2007 end-page: 3194 publication-title: J Exp Med – volume: 141 start-page: 133 year: 2014 end-page: 142 publication-title: Immunology – volume: 168 start-page: 412 year: 2013 end-page: 421 publication-title: Br J Dermatol – volume: 433 start-page: 532 year: 2011 end-page: 537 publication-title: Biochem Biophys Res Commun – volume: 11 start-page: 763 year: 2012 end-page: 776 publication-title: Nat Rev Drug Discov – volume: 366 start-page: 1181 year: 2012 end-page: 1189 publication-title: N Engl J Med – volume: 5 start-page: e14108 year: 2010 publication-title: PLoS ONE – volume: 366 start-page: 1190 year: 2012 end-page: 1199 publication-title: N Engl J Med – volume: 181 start-page: 669 year: 2008 end-page: 679 publication-title: J Immunol – volume: 2 start-page: 52ra72 year: 2010 publication-title: Sci Transl Med – volume: 371 start-page: 1675 year: 2008 end-page: 1684 publication-title: Lancet – volume: 168 start-page: 1294 year: 2013 end-page: 1302 publication-title: Br J Dermatol – ident: e_1_2_10_23_1 doi: 10.1038/ni.2797 – ident: e_1_2_10_20_1 doi: 10.1111/bjd.12236 – ident: e_1_2_10_4_1 doi: 10.1084/jem.20071094 – ident: e_1_2_10_14_1 doi: 10.1111/j.1600-6143.2011.03867.x – ident: e_1_2_10_27_1 doi: 10.1182/blood.V98.12.3309 – ident: e_1_2_10_2_1 doi: 10.1016/j.it.2012.11.005 – ident: e_1_2_10_19_1 doi: 10.1038/nrd3794 – ident: e_1_2_10_29_1 doi: 10.4049/jimmunol.181.1.669 – ident: e_1_2_10_3_1 doi: 10.1056/NEJMra0804595 – ident: e_1_2_10_22_1 doi: 10.1038/jid.2010.432 – ident: e_1_2_10_10_1 doi: 10.1111/bjd.12112 – ident: e_1_2_10_18_1 doi: 10.1111/imm.12142 – ident: e_1_2_10_30_1 doi: 10.1016/j.bbrc.2013.03.024 – ident: e_1_2_10_9_1 doi: 10.1111/bjd.12110 – ident: e_1_2_10_21_1 doi: 10.1038/jid.2013.526 – ident: e_1_2_10_28_1 doi: 10.1111/j.1744-9987.2012.01109.x – ident: e_1_2_10_26_1 doi: 10.4049/jimmunol.1200385 – ident: e_1_2_10_8_1 doi: 10.1056/NEJMoa1109017 – ident: e_1_2_10_13_1 doi: 10.1111/j.1365-2133.2008.08769.x – ident: e_1_2_10_5_1 doi: 10.1126/scitranslmed.3001107 – ident: e_1_2_10_15_1 doi: 10.1016/j.jaci.2012.04.024 – ident: e_1_2_10_24_1 doi: 10.1002/jlb.66.6.989 – ident: e_1_2_10_12_1 doi: 10.1371/journal.pone.0014108 – ident: e_1_2_10_11_1 doi: 10.4049/jimmunol.1100123 – ident: e_1_2_10_32_1 doi: 10.1111/j.1601-0825.2010.01704.x – ident: e_1_2_10_6_1 doi: 10.1056/NEJMoa1109997 – ident: e_1_2_10_16_1 doi: 10.1056/NEJMoa1314258 – ident: e_1_2_10_17_1 doi: 10.1111/j.1365-2133.2008.08902.x – ident: e_1_2_10_25_1 doi: 10.1084/jem.20132413 – ident: e_1_2_10_7_1 doi: 10.1016/S0140-6736(08)60726-6 – ident: e_1_2_10_31_1 doi: 10.1038/jid.2010.340 – reference: 22455412 - N Engl J Med. 2012 Mar 29;366(13):1181-9 – reference: 21124836 - PLoS One. 2010;5(11):e14108 – reference: 22151104 - Am J Transplant. 2012 Feb;12(2):504-5; author reply 506 – reference: 11719368 - Blood. 2001 Dec 1;98(12):3309-14 – reference: 22566565 - J Immunol. 2012 Jun 15;188(12):6287-99 – reference: 23330679 - Br J Dermatol. 2013 Jun;168(6):1294-302 – reference: 23819583 - Immunology. 2014 Feb;141(2):133-42 – reference: 25007392 - N Engl J Med. 2014 Jul 24;371(4):326-38 – reference: 22677045 - J Allergy Clin Immunol. 2012 Jul;130(1):145-54.e9 – reference: 18566434 - J Immunol. 2008 Jul 1;181(1):669-79 – reference: 19016708 - Br J Dermatol. 2009 Feb;160(2):319-24 – reference: 23023676 - Nat Rev Drug Discov. 2012 Oct;11(10):763-76 – reference: 21085185 - J Invest Dermatol. 2011 Mar;131(3):677-87 – reference: 10614782 - J Leukoc Biol. 1999 Dec;66(6):989-95 – reference: 21289639 - J Invest Dermatol. 2011 May;131(5):1110-8 – reference: 18039949 - J Exp Med. 2007 Dec 24;204(13):3183-94 – reference: 23106107 - Br J Dermatol. 2013 Feb;168(2):412-21 – reference: 23362969 - Br J Dermatol. 2013 Feb;168(2):402-11 – reference: 23046369 - Ther Apher Dial. 2012 Oct;16(5):445-8 – reference: 20926833 - Sci Transl Med. 2010 Oct 6;2(52):52ra72 – reference: 23291100 - Trends Immunol. 2013 Apr;34(4):174-81 – reference: 24913232 - J Exp Med. 2014 Jun 30;211(7):1307-14 – reference: 22455413 - N Engl J Med. 2012 Mar 29;366(13):1190-9 – reference: 18684158 - Br J Dermatol. 2008 Nov;159(5):1092-102 – reference: 23524263 - Biochem Biophys Res Commun. 2013 Apr 19;433(4):532-7 – reference: 18486740 - Lancet. 2008 May 17;371(9625):1675-84 – reference: 24362892 - Nat Immunol. 2014 Feb;15(2):143-51 – reference: 24317395 - J Invest Dermatol. 2014 May;134(5):1276-84 – reference: 19641206 - N Engl J Med. 2009 Jul 30;361(5):496-509 – reference: 21606249 - J Immunol. 2011 Jul 1;187(1):490-500 – reference: 20646232 - Oral Dis. 2011 Jan;17(1):60-7 |
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| Snippet | The response of psoriasis to antibodies targeting the interleukin (IL)‐23/IL‐17A pathway suggests a prominent role of T‐helper type‐17 (Th17) cells in this... The response of psoriasis to antibodies targeting the interleukin ( IL )‐23/ IL ‐17A pathway suggests a prominent role of T‐helper type‐17 (Th17) cells in this... The response of psoriasis to antibodies targeting the interleukin (IL)-23/IL-17A pathway suggests a prominent role of T-helper type-17 (Th17) cells in this... |
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| SubjectTerms | Adolescent Adult Aged Antibodies, Monoclonal - administration & dosage Antibodies, Monoclonal - adverse effects Cell Communication - immunology Dose-Response Relationship, Immunologic Humans IL-17A Interleukin-17 - antagonists & inhibitors Keratinocytes - immunology Keratinocytes - pathology Middle Aged neutrophils Neutrophils - immunology Neutrophils - pathology Original psoriasis Psoriasis - immunology Psoriasis - pathology Psoriasis - therapy secukinumab Time Factors Young Adult |
| Title | Evidence that a neutrophil-keratinocyte crosstalk is an early target of IL-17A inhibition in psoriasis |
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