Skin Barrier Abnormalities and Immune Dysfunction in Atopic Dermatitis.
Allergens
Animals
Biomarkers
Cytokines
/ metabolism
Dermatitis, Atopic
/ etiology
Disease Management
Disease Susceptibility
/ immunology
Homeostasis
Humans
Immunity
Immunomodulation
Lymphocyte Subsets
/ immunology
Signal Transduction
Skin
/ immunology
Toll-Like Receptors
/ metabolism
Thymic Stromal Lymphopoietin
atopic dermatitis
homeostasis
immunity
skin
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:
20 Apr 2020
20 Apr 2020
Historique:
received:
30
03
2020
revised:
14
04
2020
accepted:
17
04
2020
entrez:
25
4
2020
pubmed:
25
4
2020
medline:
23
1
2021
Statut:
epublish
Résumé
Atopic dermatitis (AD) is a common and relapsing skin disease that is characterized by skin barrier dysfunction, inflammation, and chronic pruritus. While AD was previously thought to occur primarily in children, increasing evidence suggests that AD is more common in adults than previously assumed. Accumulating evidence from experimental, genetic, and clinical studies indicates that AD expression is a precondition for the later development of other atopic diseases, such as asthma, food allergies, and allergic rhinitis. Although the exact mechanisms of the disease pathogenesis remain unclear, it is evident that both cutaneous barrier dysfunction and immune dysregulation are critical etiologies of AD pathology. This review explores recent findings on AD and the possible underlying mechanisms involved in its pathogenesis, which is characterized by dysregulation of immunological and skin barrier integrity and function, supporting the idea that AD is a systemic disease. These findings provide further insights for therapeutic developments aiming to repair the skin barrier and decrease inflammation.
Identifiants
pubmed: 32326002
pii: ijms21082867
doi: 10.3390/ijms21082867
pmc: PMC7215310
pii:
doi:
Substances chimiques
Allergens
0
Biomarkers
0
Cytokines
0
Toll-Like Receptors
0
Thymic Stromal Lymphopoietin
GT0IL38SP4
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Research Foundation of Korea
ID : NRF-2019R1A2C2085739
Organisme : National Research Foundation of Korea
ID : NRF-2020R1A4A2002894
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