The IL31 gene encodes Interleukin-31, a pleiotropic inflammatory cytokine primarily produced by activated T helper 2 (Th2) cells, but also by mast cells, macrophages, and dendritic cells. It functions by binding to a heterodimeric receptor complex composed of Interleukin-31 receptor alpha (IL-31RA) and Oncostatin M Receptor (OSMR), which are constitutively expressed on various cell types, including epithelial cells, keratinocytes, monocytes, and subsets of neurons in dorsal root ganglia ^[1-2]. This binding activates intracellular signaling pathways such as JAK/STAT, PI3K/AKT, and MAPK, leading to functions in regulating hematopoiesis, immune responses, and the induction of chemokines and pro-inflammatory cytokines ^[1]. IL-31 is strongly associated with pruritic (itchy) skin diseases like atopic dermatitis (eczema), allergic contact dermatitis, prurigo nodularis, and bullous pemphigoid, playing a key role in the sensation of itch ^[3]. It has also been implicated in other conditions such as asthma, allergic rhinitis, inflammatory bowel disease, systemic lupus erythematosus, rheumatoid arthritis, vitiligo, and various cancers (e.g., follicular lymphoma, endometrial cancer, hepatocellular carcinoma) ^[4].

The huIL31(BALB/c) mouse is a humanized model, constructed by replacing the sequences from the ATG start codon to the TGA stop codon of the endogenous mouse Il31 gene with the sequences from the ATG start codon to the TAA stop codon of the human IL31 gene. This model can be used for the research on the pathogenesis of various pruritic skin diseases, inflammatory diseases, and cancers, as well as the development of IL31-targeted drugs.