Technical Articles

Atopic dermatitis is a common chronic inflammatory skin disease characterized by dry skin, severe itching, and impaired epidermal barrier function.

Protein-labeled receptors, as the molecular cornerstone for organisms to perceive the environment and regulate functions, exemplify the translational path from basic science to clinical medicine. Every deeper understanding of receptor structure and function directly translates into clearer insights into disease mechanisms and more precise therapeutic tools.

Interleukin-13 is a core effector cytokine of type 2 immune responses, secreted by activated Th2 cells, type 2 innate lymphoid cells, and others.

The mechanism by which IL-13 targeted therapy affects paradoxical erythema at the molecular level is still unclear, and further basic research is needed from the perspectives of immune microenvironment and receptor regulation.

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by severe itching and eczema like skin lesions, which seriously affect the quality of life of patients. Its pathogenesis involves immune regulation abnormalities, among which interleukin-13 (IL-13) plays a central role in driving type 2 inflammatory response.

Atopic dermatitis (AD) is a common chronic inflammatory skin disease characterized by intense pruritus and recurrent eczematous lesions. In recent years, with the deepening understanding of AD pathogenesis, scientists have discovered that various cytokines and signaling pathways play pivotal roles in the disease process, providing a theoretical basis for the development of novel therapeutic targets.