Tristetraprolin expression by keratinocytes ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Title :
Tristetraprolin expression by keratinocytes controls local and systemic inflammation
Author(s) :
Andrianne, Mathieu [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Assabban, Assiya [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
La, Caroline [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Mogilenko, Denis [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Salle, Delphine Staumont [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Fleury, Sébastien [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Doumont, Gilles [Auteur]
Université libre de Bruxelles [ULB]
van Simaeys, Gaëtan [Auteur]
Université libre de Bruxelles [ULB]
Nedospasov, Sergei [Auteur]
Lomonosov Moscow State University = Université d'État Lomonossov de Moscou [Moscou] [MSU]
Engelhardt Institute of Molecular Biology [ISTC]
Dombrowicz, David [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Blackshear, Perry [Auteur]
Duke University Medical Center
National Institute of Environmental Health Sciences [Durham, NC, USA] [NIEHS-NIH]
Goriely, Stanislas [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Van Maele, Laurye [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Assabban, Assiya [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
La, Caroline [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Mogilenko, Denis [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Salle, Delphine Staumont [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Fleury, Sébastien [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Doumont, Gilles [Auteur]
Université libre de Bruxelles [ULB]
van Simaeys, Gaëtan [Auteur]
Université libre de Bruxelles [ULB]
Nedospasov, Sergei [Auteur]
Lomonosov Moscow State University = Université d'État Lomonossov de Moscou [Moscou] [MSU]
Engelhardt Institute of Molecular Biology [ISTC]
Dombrowicz, David [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Blackshear, Perry [Auteur]
Duke University Medical Center
National Institute of Environmental Health Sciences [Durham, NC, USA] [NIEHS-NIH]
Goriely, Stanislas [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Van Maele, Laurye [Auteur]
Université libre de Bruxelles [ULB]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
Journal title :
JCI Insight
Pages :
e92979
Publisher :
American Society for Clinical Investigation
Publication date :
2017-06-02
ISSN :
2379-3708
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Tristetraprolin (TTP, encoded by the Zfp36 gene) regulates the mRNA stability of several important cytokines. Due to the critical role of this RNA-binding protein in the control of inflammation, TTP deficiency leads to the ...
Show more >Tristetraprolin (TTP, encoded by the Zfp36 gene) regulates the mRNA stability of several important cytokines. Due to the critical role of this RNA-binding protein in the control of inflammation, TTP deficiency leads to the spontaneous development of a complex inflammatory syndrome. So far, this phenotype has been largely attributed to dysregulated production of TNF and IL‑23 by myeloid cells, such as macrophages or DCs. Here, we generated mice with conditional deletion of TTP in keratinocytes (Zfp36fl/flK14-Cre mice, referred to herein as Zfp36ΔEP mice). Unlike DC-restricted (CD11c-Cre) or myeloid cell-restricted (LysM-Cre) TTP ablation, these mice developed exacerbated inflammation in the imiquimod-induced psoriasis model. Furthermore, Zfp36ΔEP mice progressively developed a spontaneous pathology with systemic inflammation, psoriatic-like skin lesions, and dactylitis. Finally, we provide evidence that keratinocyte-derived TNF production drives these different pathological features. In summary, these findings expand current views on the initiation of psoriasis and related arthritis by revealing the keratinocyte-intrinsic role of TTP.Show less >
Show more >Tristetraprolin (TTP, encoded by the Zfp36 gene) regulates the mRNA stability of several important cytokines. Due to the critical role of this RNA-binding protein in the control of inflammation, TTP deficiency leads to the spontaneous development of a complex inflammatory syndrome. So far, this phenotype has been largely attributed to dysregulated production of TNF and IL‑23 by myeloid cells, such as macrophages or DCs. Here, we generated mice with conditional deletion of TTP in keratinocytes (Zfp36fl/flK14-Cre mice, referred to herein as Zfp36ΔEP mice). Unlike DC-restricted (CD11c-Cre) or myeloid cell-restricted (LysM-Cre) TTP ablation, these mice developed exacerbated inflammation in the imiquimod-induced psoriasis model. Furthermore, Zfp36ΔEP mice progressively developed a spontaneous pathology with systemic inflammation, psoriatic-like skin lesions, and dactylitis. Finally, we provide evidence that keratinocyte-derived TNF production drives these different pathological features. In summary, these findings expand current views on the initiation of psoriasis and related arthritis by revealing the keratinocyte-intrinsic role of TTP.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
ANR Project :
Source :
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