Background: The ”internal and external crosstalk” between skin barrier dysfunction and immune inflammatory response is the main pathogenesis of atopic dermatitis (AD), with the Th2 immune inflammatory response being the main link. Migration of circulating lymphocytes to inflammatory sites is essential for the immune response. Although AD is characterized by lymphocyte infiltration into the dermis, its skin-homing effect remains poorly defined. Methods: In this study, we induced an AD mouse model using DNFB to observe the skin barrier function changes and examine the Th2 immune inflammatory response. Additionally, we analyzed the homing of Th2 cells from peripheral blood to the skin and the gene and protein expression of key homing molecules. Furthermore, we explored the relationship between skin-homing and AD. Results: In the AD mouse model, skin barrier damage was observed, along with the skin-homing of Th2 lymphocytes and related immune inflammatory responses. Correlation analysis showed a significant positive correlation between the levels of homing cells and homing molecule proteins in peripheral blood and the protein levels of skin Th2 immune cells and transcription factors. Additionally, there was a significant linear relationship between the gene levels of homing molecules and AD symptoms. Conclusions: This study found that AD mice mainly exhibited skin barrier damage and Th2 cell immune responses, along with the phenomenon of skin-homing of Th2 lymphocytes, which can exacerbate AD symptoms. By intervening in the skin-homing of Th2 lymphocytes, AD symptoms can be effectively improved, and recurrences could be prevented.

Background: The ”internal and external crosstalk” between skin barrier dysfunction and immune inflammatory response is the main pathogenesis of atopic dermatitis (AD), with the Th2 immune inflammatory response being the main link. Migration of circulating lymphocytes to inflammatory sites is essential for the immune response. Although AD is characterized by lymphocyte infiltration into the dermis, its skin-homing effect remains poorly defined. Methods: In this study, we induced an AD mouse model using DNFB to observe the skin barrier function changes and examine the Th2 immune inflammatory response. Additionally, we analyzed the homing of Th2 cells from peripheral blood to the skin and the gene and protein expression of key homing molecules. Furthermore, we explored the relationship between skin-homing and AD. Results: In the AD mouse model, skin barrier damage was observed, along with the skin-homing of Th2 lymphocytes and related immune inflammatory responses. Correlation analysis showed a significant positive correlation between the levels of homing cells and homing molecule proteins in peripheral blood and the protein levels of skin Th2 immune cells and transcription factors. Additionally, there was a significant linear relationship between the gene levels of homing molecules and AD symptoms. Conclusions: This study found that AD mice mainly exhibited skin barrier damage and Th2 cell immune responses, along with the phenomenon of skin-homing of Th2 lymphocytes, which can exacerbate AD symptoms. By intervening in the skin-homing of Th2 lymphocytes, AD symptoms can be effectively improved, and recurrences could be prevented.