146 miR-31 and IL-34 expression are regulated in response to DNFB in the contact hypersensitivity mouse model

Contact allergy to at least one allergen is common in the European population with a prevalence of 27%. It can develop into allergic contact dermatitis (ACD), which an inflammatory skin condition characterized as delayed-type hypersensitivity reaction manifesting rash and it known that allergen-specific tissue-resident memory CD8+ T (TRM) cells are important development ACD. has been previously shown IL-34 contributes maintenance specific immune tissue-specific manner. Interestingly, only miRNA target miR-31. We aimed study role miR-31 context ACD TRM cells. In this study, mouse model was used where mice were sensitized on ears DNFB challenged after minimum 21 days DNFB. As expected challenge led increase ear thickness number epidermis. Our results show decreased expression its gene Il34 receptors Sdc1, Csf1r, Ptprz1 epidermis upon To determine cell types responsible for change we analyzed sorted stimulated keratinocytes able detect miR-31, Il34, increased Csf1r group. Interestingly primary keratinocytes, stimulation downregulated both RNA protein levels. demonstrate differently regulated response Indicating different roles keratinocytes. IL34 might play pathogenesis by regulating viability