Thymic stromal lymphopoietin (TSLP) acts as a crucial pathogenic factor in the progression of atopic dermatitis (AD). TSLP is highly expressed in keratinocytes within lesioned skin of patients with acute and chronic AD, whereas it is barely detectable in healthy human skin and non-lesioned skin from AD patients. Further studies have demonstrated that allergic inflammation is initiated by TSLP, which stimulates, activates and mobilizes Langerhans cells to skin-draining lymph nodes to trigger subsequent immune responses. Meanwhile, elevated expression of cytokines including IL‑1β, IL‑13, IL‑4 and TNF-α is detected in damaged skin of AD patients, and these cytokines in turn promote TSLP production. Dysregulated TSLP in AD is closely associated with the deficiency of Notch signaling. In animal models, epithelial keratinocyte-specific Notch deletion impairs skin barrier integrity and forms a wound-like microenvironment. Upregulated TSLP mediates Th2-dominant inflammatory immunity, leading to AD-like skin lesions in mice. In addition, specific deletion of retinoid X receptor α (RXRα) and RXRβ in mouse keratinocytes also induces AD-like dermatitis via TSLP upregulation.

Female Balb/c mice, 6 weeks old
Modeling method: Mice were subcutaneously injected with TSLP into the right ear on days 0, 2, 4 and 7. The atopic dermatitis model was successfully established 6 hours after the last injection.
Evaluation indexes: general observation and ear weight measurement, ELISA detection, HE staining

General observation and ear weight measurement

ELISA detection

Skin tissue HE staining