Keratinocyte-intrinsic BCL10/MALT1 activity initiates and amplifies psoriasiform skin inflammation.
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
26 Nov 2021
26 Nov 2021
Historique:
entrez:
26
11
2021
pubmed:
27
11
2021
medline:
8
3
2022
Statut:
ppublish
Résumé
Psoriasis is a chronic inflammatory skin disease arising from poorly defined pathological cross-talk between keratinocytes and the immune system. BCL10 (B cell lymphoma/leukemia 10) and MALT1 (mucosa-associated lymphoid tissue lymphoma translocation protein 1) are ubiquitously expressed inflammatory signaling proteins that can interact with the psoriasis susceptibility factor CARD14, but their functions in psoriasis are insufficiently understood. We report that although keratinocyte-intrinsic BCL10/MALT1 deletions completely rescue inflammatory skin pathology triggered by germline
Identifiants
pubmed: 34826258
doi: 10.1126/sciimmunol.abi4425
doi:
Substances chimiques
B-Cell CLL-Lymphoma 10 Protein
0
Bcl10 protein, mouse
0
Malt1 protein, mouse
EC 3.4.22.-
Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
EC 3.4.22.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM