Abstract
Interleukin-35 (IL-35), a member of the IL-12 family, functions as a new anti-inflammatory factor involved in arthritis, psoriasis, inflammatory bowel disease (IBD) and other immune diseases. Although IL-35 can significantly prevent the development of inflammation in many diseases, there have been no early studies accounting for the role of IL-35 recombinant protein in IBD and psoriasis. In this study, we assessed the therapeutic potential of IL-35 recombinant protein in three well-known mouse models: the dextransulfate sodium (DSS)-induced colitis mouse model, the keratin14 (K14)-vascular endothelial growth factor A (VEGF-A)-transgenic (Tg) psoriasis mouse model and the imiquimod (IMQ)-induced psoriasis mouse model. Our results indicated that IL-35 recombinant protein can slow down the pathologic process in DSS-induced acute colitis mouse model by decreasing the infiltrations of macrophages, CD4(+) T and CD8(+) T cells and by promoting the infiltration of Treg cells. Further analysis demonstrated that IL-35 recombinant protein may regulate inflammation through promoting the secretion of IL-10 and inhibiting the expression of pro-inflammatory cytokines such as IL-6, TNF-α and IL-17 in acute colitis model. In addition, lower dose of IL-35 recombinant protein could achieve long-term treatment effects as TNF-α monoclonal antibody did in the psoriasis mouse. In summary, the remarkable therapeutic effects of IL-35 recombinant protein in acute colitis and psoriasis mouse models indicated that IL-35 recombinant protein had a variety of anti-inflammatory effects and was expected to become an effective candidate drug for the treatment of inflammatory diseases.