.png){kind=icon}
.png){kind=icon}
Return
A shift towards a type I immune response in chronic atopic dermatitis favours an IL-15 dependent tissue resident memory cell niche
.png){kind=icon}
OA
AI
A
C
A
S
M
D
M
DOI：10.1016/j.jdermsci.2026.04.004.png)
.png){kind=icon}
.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
• Keratinocytes are the main epidermal source of IL-15, induced by IFNγ • Fibroblasts contribute under long-term IL-4 exposure, suggesting delayed dermal IL-15 response. • IL-15 expression associates with IFN signature, longer disease duration, TRM markers (CCR8, CD69) • Chronic AD: shift from Th2- to IFN-dominated inflammation, creating a TRM-supportive niche • IL-15 acts as bridge between IFN-driven inflammation and TRM persistence → eczema chronification.
Keywords:
TRM
atopic dermatitis
skin immunity
type I Immune response
IL-15
chronification
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.
Journal
IF:
4
Papers:
3.6K
Citations:
6.4K
Organization
Cited Papers