Keratinocyte Expression of A20/TNFAIP3 ...
Type de document :
Compte-rendu et recension critique d'ouvrage
Titre :
Keratinocyte Expression of A20/TNFAIP3 Controls Skin Inflammation Associated with Atopic Dermatitis and Psoriasis
Auteur(s) :
Devos, Michael [Auteur]
Mogilenko, Denis [Auteur]
Fleury, Sébastien [Auteur]
Gilbert, Barbara [Auteur]
Becquart, Coralie [Auteur]
Quemener, Sandrine [Auteur]
Dehondt, Hélène [Auteur]
Tougaard, Peter [Auteur]
Staels, Bart [Auteur]
Bachert, Claus [Auteur]
Vandenabeele, Peter [Auteur]
van Loo, Geert [Auteur]
Staumont-Salle, Delphine [Auteur]
Declercq, Wim [Auteur]
Dombrowicz, David [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U1011 [RNMCD]
Mogilenko, Denis [Auteur]
Fleury, Sébastien [Auteur]
Gilbert, Barbara [Auteur]
Becquart, Coralie [Auteur]
Quemener, Sandrine [Auteur]
Dehondt, Hélène [Auteur]
Tougaard, Peter [Auteur]
Staels, Bart [Auteur]
Bachert, Claus [Auteur]
Vandenabeele, Peter [Auteur]
van Loo, Geert [Auteur]
Staumont-Salle, Delphine [Auteur]
Declercq, Wim [Auteur]
Dombrowicz, David [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U1011 [RNMCD]
Titre de la revue :
Journal of Investigative Dermatology
Pagination :
135-145
Éditeur :
Nature Publishing Group
Date de publication :
2019-01
ISSN :
0022-202X
Mot(s)-clé(s) en anglais :
Atopic Dermatitis Psoriasis Keratinocytes Inflammatory Skin Diseases Models Mouse
Atopic Dermatitis
Psoriasis
Keratinocytes
Inflammatory Skin Diseases
Models
Mouse
Atopic Dermatitis
Psoriasis
Keratinocytes
Inflammatory Skin Diseases
Models
Mouse
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Keratinocytes are key players in chronic inflammatory skin diseases. A20 regulates NF-κBdependent expression of pro-inflammatory genes and cell death, but the impact of its expression in keratinocytes on systemic inflammation ...
Lire la suite >Keratinocytes are key players in chronic inflammatory skin diseases. A20 regulates NF-κBdependent expression of pro-inflammatory genes and cell death, but the impact of its expression in keratinocytes on systemic inflammation and skin disorders has not been determined. Comparative transcriptomic analysis of micro-dissected epidermis showed that A20 is downregulated in involved epidermis, but not in dermis, of psoriasis (Pso) and atopic dermatitis (AD) patients suggesting that loss of A20 expression in keratinocytes increases the vulnerability for Pso/AD induction. We have previously shown that epidermis-specific A20 knockout mice (A20 EKO) develop mild epidermal hyperplasia, but no macroscopic skin inflammation. We now show that various cytokines and chemokines are upregulated in A20 EKO mouse skin. A20 EKO mice also display systemic pro-inflammatory changes, even in the absence of skin immune cell infiltration, and an exacerbated disease severity upon induction of experimental Pso, AD or skin barrier disruption. Keratinocytes showed increased pro-inflammatory gene expression in the absence of A20 in unstimulated and IL-17Astimulated conditions, in part resulting from uncontrolled MyD88-dependent signaling. Our findings indicate that absence of A20 in keratinocytes leads to systemic inflammation at homeostatic conditions and is sufficient to exacerbate inflammatory skin disorders associated with different immune profiles by increasing cytokine and chemokine expression.Lire moins >
Lire la suite >Keratinocytes are key players in chronic inflammatory skin diseases. A20 regulates NF-κBdependent expression of pro-inflammatory genes and cell death, but the impact of its expression in keratinocytes on systemic inflammation and skin disorders has not been determined. Comparative transcriptomic analysis of micro-dissected epidermis showed that A20 is downregulated in involved epidermis, but not in dermis, of psoriasis (Pso) and atopic dermatitis (AD) patients suggesting that loss of A20 expression in keratinocytes increases the vulnerability for Pso/AD induction. We have previously shown that epidermis-specific A20 knockout mice (A20 EKO) develop mild epidermal hyperplasia, but no macroscopic skin inflammation. We now show that various cytokines and chemokines are upregulated in A20 EKO mouse skin. A20 EKO mice also display systemic pro-inflammatory changes, even in the absence of skin immune cell infiltration, and an exacerbated disease severity upon induction of experimental Pso, AD or skin barrier disruption. Keratinocytes showed increased pro-inflammatory gene expression in the absence of A20 in unstimulated and IL-17Astimulated conditions, in part resulting from uncontrolled MyD88-dependent signaling. Our findings indicate that absence of A20 in keratinocytes leads to systemic inflammation at homeostatic conditions and is sufficient to exacerbate inflammatory skin disorders associated with different immune profiles by increasing cytokine and chemokine expression.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Source :
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