A new study published in Clinical, Cosmetic and Investigational Dermatology investigated whether Interferon-kappa (IFN-κ)is involved in psoriasis etiology.This study recruited 20 healthy individuals, an equal number of psoriasis vulgaris patients, as well as 10 atopic dermatitis (AD). Immunohistochemistry staining, normal human epidermal keratinocytes (NHEK) culture, Ca2Cl-induced differentiation, quantitative reverse transcription (qRT-PCR)and ELISA were performed. The results revealed that the IFN-κ protein expression was extremely low in the epidermis of normal skin, but significantly increased in the suprabasal layers of epidermal keratinocytes in psoriatic skin lesions. However, IFN-κexpression in the skin lesions of AD was similar to that in normal skin. IFN-κ protein was detected in sera from psoriasis patients, but not in sera from normal and ADsubjects. In NHEK patients, the IFN-κ was notably induced by types of nucleic acid pathogen recognition receptor (PRR) agonists. Although its expression was significantly induced by itself and IFN-γ, it was inhibited by type 2 immunity cytokines interleukin (IL)4 and IL13. Whereas, other inflammatory cytokines including IL1 super-family members and IL17A did not alter its expression. Furthermore, the addition of recombinant IFN-κ did not affect keratinocytes differentiation.In inference, it was stated that increased IFN-κ in psoriasis may be caused by injured cells-released nucleic acids, increased IFN-γ and self-activation. Its enhancement may contribute to the etiology of the disease byenhancing TNFA and IL17A gene expressions.