337 JAML propels the inflammatory responses to contact allergens

Allergic contact dermatitis (ACD) is a skin disease with complex pathophysiology. It well established that epidermal-resident memory CD8+ T (CD8+ TRM) cells are responsible for the rapid flare-up reaction and production of IFNγ IL-17A seen after challenge allergens. Nevertheless, pathways kick off their effector functions unclear. Junctional adhesion molecule-like protein (JAML) was recently described as important in promoting tumor-infiltrating cells, but its role ACD unknown. To examine JAML’s local inflammatory response to allergens, we used various mouse models JAML knockout (KO) wild-type (WT) mice. The ear thickness reduced by 50% (p<0.0001) KO mice compared WT concomitant significant decrease CXCL2 CXCL5 following experimental allergen 1-fluoro-2,4-dinitrobenzene (DNFB). We found 68±7% TRM express loss leads decreased numbers IFNγ-producing TRMcells approximately 2-fold (p=0.0258). Finally, analyzing three publicly available gene expression datasets, show patients exhibit increased skin. Together, our study first present an essential responses allergens enlighten new possible target treatment ACD.