- Due to immune dysregulation, non-lesional AD skin is characterized by subclinical inflammation as well as skin-barrier dysfunction1
- Dendritic cells take up antigens and amplify type 2 immunity cytokines1
- Worsened skin-barrier dysfunction can stimulate keratinocytes to further promote type 2 inflammation through the release of skin alarmins, such as IL-25, IL-33, and TSLP, which stimulate ILC2s to release more type 2 cytokines such as IL-13 and IL-5 1
Acute Lesional Skin
- Acute lesional skin is characterized by a reduced expression of important skin-barrier proteins and lipids involved in maintaining skin-barrier integrity1
- The damage caused to the skin barrier triggers the release of further skin alarmins, expanding and activating skin-resident ILC2 cells to produce more cytokines, attracting more immune cells, and amplifying the inflammatory response, including the recruitment of more eosinophils, Th2 cells, and Th22 cells— producing more cytokines1
- Both IL-33 and TSLP, as well as the downstream Th2 cytokines (IL-4, IL-13, and IL-31), act directly on cutaneous sensory neurons, activating itch signaling and leading to scratching1
- During an AD flare there is a decreased microbial diversity, with increased presence of Staphylococcus aureus1
Chronic Lesional Skin
- In the chronic stage, a mixed T-cell infiltrate, including Th1 and Th17 cells, perpetuates skin inflammation and promotes skin remodeling and fibrosis1
- Repetitive scratching leads to lichenified (thickened) skin1
ILC, innate lymphoid cell; TSLP, thymic stromal lymphopoietin.
IL-13, plays a key role in atopic dermatitis signs and symptoms, including skin barrier defects and infections, inflammation, skin thickening, and promoting the
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