Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritus and eczema. It is influenced by both genetic and environmental factors, involving immune dysregulation and skin barrier dysfunction. In our lab, we focus on understanding the pathophysiology of AD, particularly through the investigation of immune responses, skin barrier repair mechanisms, and the role of specific cytokines. Our work aims to identify novel therapeutic targets to improve the management of AD and its associated comorbidities.
사진) 클립아트코리아 

Immunodermatology studies the complex interactions between the immune system and the skin, particularly in diseases with immune-mediated pathologies. Our lab investigates the mechanisms underlying various immunodermatological diseases, including autoimmune skin disorders and allergic reactions. Through innovative approaches like high-dimensional tissue imaging and mouse models, we aim to uncover the cellular and molecular pathways that drive skin inflammation and immune response in dermatologic diseases. 

Tissue-resident memory T cells (TRM) are a subset of memory T cells that reside in peripheral tissues, such as the skin, where they play a crucial role in immune surveillance and response to local infections. In our research, we explore the function and differentiation of TRM cells in the skin, especially in the context of skin inflammation and autoimmune diseases. Understanding TRM dynamics could provide insights into tissue-specific immunity and potential strategies for enhancing immune protection or modulating autoimmune responses in the skin. 

Itch is a hallmark symptom of atopic dermatitis (AD) and other chronic inflammatory skin conditions. Itch sensation is often mediated by the interaction between sensory neurons in the dorsal root ganglia (DRG) and immune cells. Our lab focuses on unraveling the neuroimmune mechanisms of itch in AD, with an emphasis on the role of sensory neurons and their interaction with immune cells. By understanding the molecular pathways of itch, we aim to develop targeted treatments to alleviate this debilitating symptom in patients with AD and other pruritic skin disease.

The skin serves as an important neuroimmune interface where sensory neurons, immune cells, and resident skin cells continuously communicate to maintain tissue homeostasis. Disruption of this communication plays a central role in the pathogenesis of inflammatory skin diseases, including atopic dermatitis (AD), leading to chronic inflammation, barrier dysfunction, and persistent itch. Understanding these neuroimmune interactions provides new insights into disease mechanisms and offers opportunities for the development of targeted therapies for chronic inflammatory skin disorders. 

Atopic march refers to the progression of allergic diseases, beginning with atopic dermatitis in infancy and potentially leading to asthma and allergic rhinitis later in life. The mechanisms behind the atopic march remain poorly understood, but our research investigates how early-life immune responses and environmental exposures contribute to this progression. We aim to identify biomarkers and therapeutic targets to prevent the development of allergic diseases in individuals with a history of AD, ultimately improving long-term health outcomes.