Interleukin-17A and Keratinocytes in Psoriasis.
CCL20
CXCL1
CXCL8
ILC3
Koebner phenomenon
Th17
antimicrobial peptides
interleukin-17A
keratinocytes
psoriasis
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
13 Feb 2020
13 Feb 2020
Historique:
received:
22
01
2020
revised:
11
02
2020
accepted:
11
02
2020
entrez:
20
2
2020
pubmed:
20
2
2020
medline:
20
11
2020
Statut:
epublish
Résumé
The excellent clinical efficacy of anti-interleukin 17A (IL-17A) biologics on psoriasis indicates a crucial pathogenic role of IL-17A in this autoinflammatory skin disease. IL-17A accelerates the proliferation of epidermal keratinocytes. Keratinocytes produce a myriad of antimicrobial peptides and chemokines, such as CXCL1, CXCL2, CXCL8, and CCL20. Antimicrobial peptides enhance skin inflammation. IL-17A is capable of upregulating the production of these chemokines and antimicrobial peptides in keratinocytes. CXCL1, CXCL2, and CXCL8 recruit neutrophils and CCL20 chemoattracts IL-17A-producing CCR6
Identifiants
pubmed: 32070069
pii: ijms21041275
doi: 10.3390/ijms21041275
pmc: PMC7072868
pii:
doi:
Substances chimiques
CCL20 protein, human
0
CXCL1 protein, human
0
CXCL2 protein, human
0
CXCL8 protein, human
0
Chemokine CCL20
0
Chemokine CXCL1
0
Chemokine CXCL2
0
IL17A protein, human
0
Interleukin-17
0
Interleukin-8
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : grant from The Ministry of Health, Labour, and Welfare in Japan
ID : H30-Shokuhin-Shitei-005
Déclaration de conflit d'intérêts
The authors have no conflicts of interest.
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