MyD88 signaling in T regulatory cells by endogenous ligands dampens skin inflammation in filaggrin deficient mice

MyD88 signaling in T regulatory cells by endogenous ligands dampens skin inflammation in filaggrin deficient mice

Copyright © 2018 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 195(2018) vom: 25. Okt., Seite 88-92
1. Verfasser: Hoff, Sabine (VerfasserIn)
Weitere Verfasser: Oyoshi, Michiko K, Hornick, Jason L, Geha, Raif S, NIH/NIAID funded Atopic Dermatitis Research Network
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2018
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't FLG protein, human Filaggrin Proteins Interleukin-17 Interleukins Intermediate Filament Proteins Myeloid Differentiation Factor 88
Beschreibung
Zusammenfassung:Copyright © 2018 Elsevier Inc. All rights reserved.
Mutations in filaggrin are associated with atopic dermatitis. Filaggrin-deficient flaky tail (Flgft/ft) mice develop spontaneous inflammatory skin lesion that wax and wane. We show that loss of MyD88 promotes the persistence of skin lesions in Flgft/ft mice and exaggerates their expression of the Th17-associated cytokines Il7a and Il22. The development and persistence of skin lesions in Flgft/ft mice was independent of the microbiota. MyD88-mediated signals are shown to be important for the accumulation of T regulatory cells (Tregs) in lesional skin of Flgft/ft mice. Adoptive transfer of WT Tregs dampened the severity of skin lesions in MyD88-/-/Flgft/ft mice. These results suggest that MyD88 signaling in Treg cells by endogenous ligands attenuates skin inflammation in filaggrin deficiency
Beschreibung:Date Completed 27.08.2019
Date Revised 13.12.2023
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2018.08.001