Allergic diseases such as allergic rhinitis, asthma, and atopic dermatitis are characterized by an exaggerated immune response to otherwise harmless environmental proteins found in pollen, house dust mites, mold, cockroach debris, and pet dander. The immune system’s failure to maintain tolerance towards these allergens triggers a cascade of immune events, leading to chronic inflammation and tissue damage.

At the heart of allergic pathology is the intricate interaction between innate and adaptive immune cells, which coordinates the body's response to allergens. Key players in this process are T-helper type 2 (Th2) cells, a subset of T cells that orchestrate many of the immune mechanisms driving allergic inflammation.

Upon exposure to allergens, dendritic cells capture and process allergen-derived antigens, presenting them to naïve T cells in lymphoid tissues. In genetically or environmentally susceptible individuals, these naïve T cells differentiate into Th2 cells, which produce cytokines such as IL-4, IL-5, IL-9, and IL-13. These T cell-derived cytokines promote the production of IgE antibodies by B cells, sensitizing mast cells and basophils to allergens.

Additionally, these cytokines induce the activation and recruitment of eosinophils. Mast cells, basophils, and eosinophils then release mediators like histamine and proteases, leading to inflammation and allergic symptoms. Moreover, Th2 cells maintain a feedback loop that perpetuates chronic inflammation, contributing to conditions such as asthma, allergic rhinitis, and atopic dermatitis. Understanding the underlying immune mechanisms that lead to Th2 responses and their maintenance is crucial for developing novel therapeutic strategies to prevent and treat allergic conditions.

Our research team is dedicated to uncovering the fundamental mechanisms of airway and cutaneous allergic inflammation, primarily using mouse models. We focus on understanding how environmental allergens trigger and sustain allergic diseases, with particular attention to interactions between innate immune cells—such as monocytes, macrophages, and dendritic cells—and adaptive immune responses, especially Th2 cells. We explore how these immune interactions are influenced by the nature of allergens, environmental exposures, genetic factors, and microbiota.

Additionally, we investigate how these processes vary during sensitive periods, such as infancy and pregnancy, to better understand the onset and persistence of allergic inflammation. To advance our knowledge, we utilize advanced techniques, including conditional knockout murine models, multi-color flow cytometry, histology, functional lung assessment, microscopy, RNA-Seq, and single-cell technologies. Our ultimate goal is to identify targets for preventing or treating human allergic diseases.