Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8721195 | Clinical Immunology | 2018 | 19 Pages |
Abstract
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 MyD88â/â/Flgft/ft mice. These results suggest that MyD88 signaling in Treg cells by endogenous ligands attenuates skin inflammation in filaggrin deficiency.
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Authors
Sabine Hoff, Michiko K. Oyoshi, Jason L. Hornick, Raif S. Geha, NIH/NIAID funded Atopic Dermatitis Research Network NIH/NIAID funded Atopic Dermatitis Research Network,