Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities
Psoriasis is a chronic, immune‐mediated, systemic inflammatory disease that is defined by a characteristic skin reaction produced when elevated levels of inflammatory cytokines such as interleukin (IL)‐17 alter the growth and differentiation of skin cells. The pathogenesis of comorbid conditions ass...
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Veröffentlicht in: | Experimental dermatology 2018-02, Vol.27 (2), p.115-123 |
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description | Psoriasis is a chronic, immune‐mediated, systemic inflammatory disease that is defined by a characteristic skin reaction produced when elevated levels of inflammatory cytokines such as interleukin (IL)‐17 alter the growth and differentiation of skin cells. The pathogenesis of comorbid conditions associated with psoriasis, including psoriatic arthritis, cardiovascular disease, obesity, metabolic syndrome, liver disorders, renal disease and depression, is also largely affected by inflammation. In this review, we examine the effect of IL‐17 on the inflammatory pathways in a variety of different cell types, including keratinocytes, as well as epithelial cells of the colon, kidney, gut and liver. Additionally, we investigate the role of IL‐17 in mediating the psoriasis‐associated comorbidities detailed above. |
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The pathogenesis of comorbid conditions associated with psoriasis, including psoriatic arthritis, cardiovascular disease, obesity, metabolic syndrome, liver disorders, renal disease and depression, is also largely affected by inflammation. In this review, we examine the effect of IL‐17 on the inflammatory pathways in a variety of different cell types, including keratinocytes, as well as epithelial cells of the colon, kidney, gut and liver. Additionally, we investigate the role of IL‐17 in mediating the psoriasis‐associated comorbidities detailed above.</description><identifier>ISSN: 0906-6705</identifier><identifier>EISSN: 1600-0625</identifier><identifier>DOI: 10.1111/exd.13467</identifier><identifier>PMID: 29152791</identifier><language>eng</language><publisher>Denmark: Wiley Subscription Services, Inc</publisher><subject>Animals ; Arthritis ; cardiovascular disease ; Cardiovascular Diseases - pathology ; Cell Differentiation ; Cell Proliferation ; Colon ; Comorbidity ; Cytokines ; Cytokines - metabolism ; Depression - pathology ; Epithelial cells ; Humans ; Hypertension - pathology ; Inflammation - pathology ; Interleukin 17 ; Interleukin-17 - metabolism ; keratinocyte ; Keratinocytes ; Keratinocytes - cytology ; Liver diseases ; Liver Diseases - pathology ; Mental depression ; Metabolic syndrome ; Metabolic Syndrome - pathology ; Mice ; obesity ; Psoriasis ; Psoriasis - pathology ; Psoriatic arthritis ; review ; Skin - pathology</subject><ispartof>Experimental dermatology, 2018-02, Vol.27 (2), p.115-123</ispartof><rights>2017 The Authors. Published by John Wiley & Sons Ltd.</rights><rights>2017 The Authors. Experimental Dermatology Published by John Wiley & Sons Ltd.</rights><rights>2018 John Wiley & Sons A/S. 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The pathogenesis of comorbid conditions associated with psoriasis, including psoriatic arthritis, cardiovascular disease, obesity, metabolic syndrome, liver disorders, renal disease and depression, is also largely affected by inflammation. In this review, we examine the effect of IL‐17 on the inflammatory pathways in a variety of different cell types, including keratinocytes, as well as epithelial cells of the colon, kidney, gut and liver. Additionally, we investigate the role of IL‐17 in mediating the psoriasis‐associated comorbidities detailed above.</description><subject>Animals</subject><subject>Arthritis</subject><subject>cardiovascular disease</subject><subject>Cardiovascular Diseases - pathology</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>Colon</subject><subject>Comorbidity</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Depression - pathology</subject><subject>Epithelial cells</subject><subject>Humans</subject><subject>Hypertension - pathology</subject><subject>Inflammation - pathology</subject><subject>Interleukin 17</subject><subject>Interleukin-17 - metabolism</subject><subject>keratinocyte</subject><subject>Keratinocytes</subject><subject>Keratinocytes - cytology</subject><subject>Liver diseases</subject><subject>Liver Diseases - pathology</subject><subject>Mental depression</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - pathology</subject><subject>Mice</subject><subject>obesity</subject><subject>Psoriasis</subject><subject>Psoriasis - pathology</subject><subject>Psoriatic arthritis</subject><subject>review</subject><subject>Skin - pathology</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp10c1qFTEYBuAgij1WF96ABNwoOG3-JpkspbZaKLhRcDdkMt_U1ExynG-mOjvvQK-xV2JOT3UhmE1-eHiT8BLylLMjXsYxfO-PuFTa3CMbrhmrmBb1fbJhlulKG1YfkEeIV4xxI039kBwIy2thLN-Qn-dphinC8iWkmx-_uKEulgOk82egXcgxX640D3R0aaUeYqTzugWkIV3neA19WdzSS0iAAXd0i3kKrmxeUVxxhjH4ooboxtHNISfqUk8dYvbBzSXB5zFPXejDHAAfkweDiwhP7uZD8vHs9MPJu-ri_dvzk9cXlVe1MpX1neCsUaoR2nEvlBiGxjbOWyvkIL2Xne2ZErV3XvsOVCedFU3fgHDMCCUPyYt97nbKXxfAuR0D7v7nEuQFW261VtJIJQt9_g-9ysuUyuuKsqLcbYwu6uVe-SkjTjC02ymMblpbztpdS21pqb1tqdhnd4lLN0L_V_6ppYDjPfgWIqz_T2pPP73ZR_4G236eqg</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Krueger, James G.</creator><creator>Brunner, Patrick M.</creator><general>Wiley Subscription Services, Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>201802</creationdate><title>Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities</title><author>Krueger, James G. ; Brunner, Patrick M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4547-9cb210844826a1c242ff898ac9923f3cc3b9d0425cac6cbe4b3a928d8e2a07243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Arthritis</topic><topic>cardiovascular disease</topic><topic>Cardiovascular Diseases - pathology</topic><topic>Cell Differentiation</topic><topic>Cell Proliferation</topic><topic>Colon</topic><topic>Comorbidity</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Depression - pathology</topic><topic>Epithelial cells</topic><topic>Humans</topic><topic>Hypertension - pathology</topic><topic>Inflammation - pathology</topic><topic>Interleukin 17</topic><topic>Interleukin-17 - metabolism</topic><topic>keratinocyte</topic><topic>Keratinocytes</topic><topic>Keratinocytes - cytology</topic><topic>Liver diseases</topic><topic>Liver Diseases - pathology</topic><topic>Mental depression</topic><topic>Metabolic syndrome</topic><topic>Metabolic Syndrome - pathology</topic><topic>Mice</topic><topic>obesity</topic><topic>Psoriasis</topic><topic>Psoriasis - pathology</topic><topic>Psoriatic arthritis</topic><topic>review</topic><topic>Skin - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krueger, James G.</creatorcontrib><creatorcontrib>Brunner, Patrick M.</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Krueger, James G.</au><au>Brunner, Patrick M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities</atitle><jtitle>Experimental dermatology</jtitle><addtitle>Exp Dermatol</addtitle><date>2018-02</date><risdate>2018</risdate><volume>27</volume><issue>2</issue><spage>115</spage><epage>123</epage><pages>115-123</pages><issn>0906-6705</issn><eissn>1600-0625</eissn><abstract>Psoriasis is a chronic, immune‐mediated, systemic inflammatory disease that is defined by a characteristic skin reaction produced when elevated levels of inflammatory cytokines such as interleukin (IL)‐17 alter the growth and differentiation of skin cells. 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subjects | Animals Arthritis cardiovascular disease Cardiovascular Diseases - pathology Cell Differentiation Cell Proliferation Colon Comorbidity Cytokines Cytokines - metabolism Depression - pathology Epithelial cells Humans Hypertension - pathology Inflammation - pathology Interleukin 17 Interleukin-17 - metabolism keratinocyte Keratinocytes Keratinocytes - cytology Liver diseases Liver Diseases - pathology Mental depression Metabolic syndrome Metabolic Syndrome - pathology Mice obesity Psoriasis Psoriasis - pathology Psoriatic arthritis review Skin - pathology |
title | Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities |
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