Atopic Dermatitis
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Atopic Dermatitis
Atopic Dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by intense itching, dry skin, and eczematous lesions. It is primarily driven by a Th2-skewed immune response and is often associated with elevated IgE levels, skin barrier dysfunction, and a strong genetic and environmental component. AD frequently begins in early childhood and can persist into adulthood, significantly affecting quality of life. Current research focuses on understanding the complex interplay between immune dysregulation, barrier defects, and microbiome imbalance to develop targeted therapies.
We has developed several atopic dermatitis mouse models that replicate human pathology, including IgE evaluation, chronic pruritus, epidermal hyperplasia, and immune cell infiltration. Our models ensure clinically translatable efficacy data for diverse drug candidates: Th2 pathway modulators, JAK inhibitors, biologics, and more. Endpoints include histopathological scoring, cytokine profiling, and molecular biomarker analysis. There are three validated AD models with distinct mechanistic profiles:
Model
DNFB-induced AD
Feature
Extrinsic AD
Hypersensitivity caused epidermal barrier-disruption
Th1 / Th17 / Th22 pathway
Model
MC903-induced AD
Feature
Extrinsic AD
TSLP/Th2 pathway
Model
OXA-induced AD
Feature
Delayed Hypersensitivity Reactions
Extrinsic AD
Th1 / Th2 / Th17 pathway
For more information:
DNFB induced AD
The DNFB-induced atopic dermatitis (AD) mouse model is uniquely constructed to exhibit robust pruritus (itch) phenotypes for enhanced therapeutic evaluation. Our models recapitulate key clinical hallmarks, including intense scratching behaviour, epidermal thickening, and Th2-skewed immune responses, ensuring translational relevance for anti-itch drug development.
The model strategy of DNFB-induced atopic dermatitis is shown in Fig.1A. After DNFB induction for 16 days, the representative photos of back skin were shown (Fig.1B). The thickness and clinical score of back skin increased significantly in the model group (Fig.1C&1D), with an accompanying increase in IgE serum levels and scratching frequency in mice after DNFB induction(Fig.1E). The mRNA expression level of type 2 cytokines including IL-33, IL-4, IL-13 and TSLP in the back skin increased significantly (Fig.1F). The results of HE staining and TB(Toluidine Blue) staining of the skin showed inflammatory cells and mast cells infiltration in the model group (Fig.1G). Data were presented by mean ± SEM. *P<0.05，**P<0.01；***P<0.001.
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