018 Evidence for IL-31/IL-31RA axis involvement in psoriasis and autoimmune skin diseases beyond atopic dermatitis and prurigo nodularis

IL-31 acts via JAK/STAT, PI3K/AKT, and MAPK pathways, leading to a wide range of immune responses alongside its pruritogenic role. Only limited data are available regarding the role in psoriasis autoimmune skin diseases. To evaluate involvement IL-31/IL-31 receptor α (IL-31RA) axis inflammatory diseases, including cutaneous lupus erythematosus(CLE), dermatomyositis(DM), systemic sclerosis(SSc), psoriasis, lichen planus(LP), we studied IL-31RA expression by immunohistochemistry (IHC) serum levels ELISA. In addition, atopic dermatitis (AD) scRNA-seq (Reynolds, 2021) was mined for cellular source IL-31/IL31RA gene expression. By IHC compared healthy control (HC) skin, lesions showed highest localized both epidermis dermal infiltrate; increased IL31RA predominantly occurred keratinocytes (p<0.01) according scRNA-seq. protein also significantly elevated infiltrate DM, LP, CLE lesions. SSc no enhancement epidermal observed, being only enhanced within infiltrate. The were higher patients than HCs, whereas significant increase observed LE, SSc. Our results suggest possible IL-31/IL-31RA inflammation beyond case AD prurigo nodularis that warrant further investigation.