Area of research
Immunology · Dermatology
Research interest
Research interests include Dermatology and Skin Diseases, Immunotherapy and Immune Responses, Cytomegalovirus and herpesvirus research, and Immune Cell Function and Interaction.
IgG autoantibodies in bullous pemphigoid induce a pathogenic MyD88-dependent pro-inflammatory response in keratinocytes
Subunit-Specific Reactivity of Autoantibodies Against Laminin-332 Reveals Direct Inflammatory Mechanisms on Keratinocytes
Characterizing the proteome of bullous pemphigoid blister fluid utilizing tandem mass tag labeling coupled with LC–MS/MS
Dysregulated microRNA expression in IL-4 transgenic mice, an animal model of atopic dermatitis
A molecular mechanism for IL-4 suppression of loricrin transcription in epidermal keratinocytes: implication for atopic dermatitis pathogenesis
Diacerein inhibits the pro-atherogenic & pro-inflammatory effects of IL-1 on human keratinocytes & endothelial cells
Aberrant Wound Healing in an Epidermal Interleukin-4 Transgenic Mouse Model of Atopic Dermatitis
Interleukin-4 Downregulation of Involucrin Expression in Human Epidermal Keratinocytes Involves Stat6 Sequestration of the Coactivator CREB-Binding Protein
Differential expression of inflammation-related genes in IL-4 transgenic mice before and after the onset of atopic dermatitis skin lesions
Interleukin‐4 up‐regulation of epidermal interleukin‐19 expression in keratinocytes involves the binding of signal transducer and activator of transcription 6 (Stat6) to the imperfect Stat6 sites
The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis
IL-4 regulates chemokine CCL26 in keratinocytes through the Jak1, 2/Stat6 signal transduction pathway: Implication for atopic dermatitis
IL-4 up-regulates epidermal chemotactic, angiogenic, and pro-inflammatory genes and down-regulates antimicrobial genes in vivo and in vitro: Relevant in the pathogenesis of atopic dermatitis
Inflammation‐Driven Dermal Lymphangiogenesis in Atopic Dermatitis is Associated with CD11b+ Macrophage Recruitment and VEGF‐C Up‐regulation in the IL‐4‐Transgenic Mouse Model