Our research focuses on uncovering the role of G protein–coupled receptor 35 (GPR35) in regulating immune responses during Epidermolysis Bullosa Acquisita (EBA), a chronic autoimmune blistering skin disease driven by neutrophil-mediated inflammation.

GPR35 is an immune-modulating receptor expressed in neutrophils, monocytes, and epithelial tissues, known for its dual role in inflammation, capable of both amplifying and resolving immune responses depending on the context. Using a hematopoietic cell–specific GPR35 knockout mouse model (Gpr35^fl/fl × Vav1-Cre), we aim to define how GPR35 influences neutrophil migration, effector functions (such as ROS release, NETosis, and lipid mediator production), and the overall progression of tissue injury in EBA.

By characterizing the signaling mechanisms of GPR35 in innate immune cells, this project seeks to identify new therapeutic strategies to control excessive inflammation and improve outcomes in autoimmune and inflammatory skin diseases.