IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis
In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that the TH17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis. We sought to understand the effect that neutralization of IL-17 has on...
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| Veröffentlicht in: | Journal of allergy and clinical immunology Jg. 130; H. 1; S. 145 - 154.e9 |
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| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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New York, NY
Mosby, Inc
01.07.2012
Elsevier Elsevier Limited |
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| ISSN: | 0091-6749, 1097-6825, 1097-6825 |
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| Abstract | In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that the TH17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis.
We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects.
We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti–IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4.
There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism.
Our data suggest that IL-17 is a key “driver” cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. |
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| AbstractList | BACKGROUND: In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that the TH17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis. OBJECTIVE: We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects. METHODS: We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti–IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4. RESULTS: There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism. CONCLUSION: Our data suggest that IL-17 is a key “driver” cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. Background In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that the TH17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis. Objective We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects. Methods We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti-IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4. Results There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF- alpha was of higher magnitude at 2 weeks than in prior studies with TNF- alpha antagonism. Conclusion Our data suggest that IL-17 is a key "driver" cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that the TH17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis. We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects. We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti–IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4. There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism. Our data suggest that IL-17 is a key “driver” cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that the T(H)17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis. We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects. We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti-IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4. There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism. Our data suggest that IL-17 is a key "driver" cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. Background In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that the TH 17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis. Objective We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects. Methods We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti–IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4. Results There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism. Conclusion Our data suggest that IL-17 is a key “driver” cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that the T(H)17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis.BACKGROUNDIn subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that the T(H)17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis.We sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects.OBJECTIVEWe sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects.We examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti-IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4.METHODSWe examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti-IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4.There were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism.RESULTSThere were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism.Our data suggest that IL-17 is a key "driver" cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis.CONCLUSIONOur data suggest that IL-17 is a key "driver" cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis. |
| Author | Cameron, Gregory S. Katcherian, Artemis Fretzin, Scott McColm, Juliet Suárez-Fariñas, Mayte Phipps, Krista M. Cueto, Inna Banerjee, Subhashis Haslett, Patrick A. Hoffman, Robert W. White, Traci Krueger, James G. |
| Author_xml | – sequence: 1 givenname: James G. surname: Krueger fullname: Krueger, James G. email: James.Krueger@rockefeller.edu organization: The Rockefeller University, New York, NY – sequence: 2 givenname: Scott surname: Fretzin fullname: Fretzin, Scott organization: Dawes Fretzin Dermatology Group, Indianapolis, Ind – sequence: 3 givenname: Mayte surname: Suárez-Fariñas fullname: Suárez-Fariñas, Mayte organization: The Rockefeller University, New York, NY – sequence: 4 givenname: Patrick A. surname: Haslett fullname: Haslett, Patrick A. organization: Eli Lilly and Company, Lilly Research Laboratories, Indianapolis, Ind – sequence: 5 givenname: Krista M. surname: Phipps fullname: Phipps, Krista M. organization: Eli Lilly and Company, Lilly Research Laboratories, Indianapolis, Ind – sequence: 6 givenname: Gregory S. surname: Cameron fullname: Cameron, Gregory S. organization: Eli Lilly and Company, Lilly Research Laboratories, Indianapolis, Ind – sequence: 7 givenname: Juliet surname: McColm fullname: McColm, Juliet organization: Eli Lilly and Company, Erl Wood, Surrey, United Kingdom – sequence: 8 givenname: Artemis surname: Katcherian fullname: Katcherian, Artemis organization: The Rockefeller University, New York, NY – sequence: 9 givenname: Inna surname: Cueto fullname: Cueto, Inna organization: The Rockefeller University, New York, NY – sequence: 10 givenname: Traci surname: White fullname: White, Traci organization: The Rockefeller University, New York, NY – sequence: 11 givenname: Subhashis surname: Banerjee fullname: Banerjee, Subhashis organization: Eli Lilly and Company, Lilly Research Laboratories, Indianapolis, Ind – sequence: 12 givenname: Robert W. surname: Hoffman fullname: Hoffman, Robert W. organization: Eli Lilly and Company, Lilly Research Laboratories, Indianapolis, Ind |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26132809$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/22677045$$D View this record in MEDLINE/PubMed |
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| Keywords | PASI Psoriasis IL-17 DEG PASI 75 DC-LAMP TH17 cells TNF At least a 75% improvement in PASI score T H17 cells Differentially expressed gene Dendritic cell-lysosomal associated membrane protein Psoriasis Area and Severity Index Human Immunopathology Skin disease Cytokine Helper cell Activation Circuit Inflammation Interleukin 17 Immunology Gene T Tumor necrosis factor Genetics 17 cells Th17 lymphocyte |
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| Snippet | In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that the TH17... Background In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that... In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that the T(H)17... Background In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that... BACKGROUND: In subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell–derived cytokines. Evidence suggests that... |
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| SubjectTerms | Allergy and Immunology Antibodies, Monoclonal - administration & dosage Antibodies, Monoclonal - immunology Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized - administration & dosage Antibodies, Monoclonal, Humanized - immunology Antibodies, Monoclonal, Humanized - therapeutic use Biological and medical sciences Chemokines Clinical trials Cloning dendritic cells Dermatology dermis dose response Dose-Response Relationship, Drug Drug dosages drugs Fundamental and applied biological sciences. Psychology Fundamental immunology Gene expression genes Humans hyperplasia IL-17 Immunopathology inflammation Inflammation - genetics Inflammation - immunology Inflammation - metabolism interleukin-17 Interleukin-17 - genetics Interleukin-17 - immunology Interleukin-17 - metabolism keratinocytes Lymphocyte Activation Lymphocytes Medical sciences messenger RNA microarray technology Molecular Sequence Data neutralization Oligonucleotide Array Sequence Analysis Pathogenesis placebos Psoriasis Psoriasis - immunology Psoriasis - physiopathology Psoriasis - therapy Psoriasis. Parapsoriasis. Lichen Reverse Transcriptase Polymerase Chain Reaction Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Skin Skin - immunology Skin - metabolism Skin - physiopathology skin lesions T-lymphocytes TH17 cells Th17 Cells - immunology TNF Treatment Outcome tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology Tumor Necrosis Factor-alpha - metabolism |
| Title | IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis |
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