Abstract
About a decade age, loss-of-function mutations in the filaggrin molecule were first implicated in the pathogenesis of ichthyosis vulgaris and, subsequently, of atopic dermatitis and other atopic diseases. Since then, intensive study of the role of filaggrin null mutations have led to other milestones in understanding the pathologic pathways in these diseases, including the initiation, maintenance, and promotion of the disease processes. The result has been new and emerging clinical and pharmacologic strategies for early identification of and intervention in atopic diseases.
Original language | English (US) |
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Pages (from-to) | 89S-91S |
Journal | Seminars in cutaneous medicine and surgery |
Volume | 35 |
DOIs | |
State | Published - Jun 1 2016 |
Keywords
- Atopic dermatitis
- Eczema
- Filaggrin
- Filaggrin null mutation
- ILC2s
- Interleukin-13
- Interleukin-25
- Nuocytes
- Toll-like receptors
- Type 2 innate lymphoid cells
ASJC Scopus subject areas
- Surgery
- Dermatology