Keratinocyte Expression of A20/TNFAIP3 ...
Document type :
Compte-rendu et recension critique d'ouvrage
Title :
Keratinocyte Expression of A20/TNFAIP3 Controls Skin Inflammation Associated with Atopic Dermatitis and Psoriasis
Author(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]
Journal title :
Journal of Investigative Dermatology
Pages :
135-145
Publisher :
Nature Publishing Group
Publication date :
2019-01
ISSN :
0022-202X
English keyword(s) :
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
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [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 ...
Show more >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.Show less >
Show more >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.Show less >
Language :
Anglais
Popular science :
Non
Source :
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