The incidence of inflammatory and autoimmune diseases has increased in the last 30 years, particularly among developed countries. Thus, there is a need for the development of novel therapies to treat these pathologies. Interleukin 23 (IL-23) is a pro-inflammatory cytokine whose excessive production plays a fundamental role in the development of several inflammatory diseases such as Crohn’s disease, ulcerative colitis, multiple sclerosis and psoriasis. The pathological consequences of excessive IL-23 signalling have been linked to its ability to promote effector functions of distinct populations of T lymphocytes: CD4 helper subset Th17 and the TCRγδ T17γδ. Despite the prominent role described for IL-23 in inflammatory diseases, the precise molecular mechanisms by which IL-23 induces pathogenic functions on T lymphocytes remain largely unknown. Our lab is interested in the characterisation of the signalling network triggered by IL-23 using novel techniques such as large-scale quantitative proteomics and phosphoproteomic approaches to uncover novel mediators of IL-23 actions. The underlying aim of this strategy is the development of novel therapeutic tools based on the interference with intracellular signalling pathways. Currently, we are characterising novel signalling mediators that link IL-23 with processes such as cell migration and metabolism. Our work extends beyond the identification of potential targets, and combines pharmacological and genetic approaches to determine the contribution of specific signalling mediators in murine models of IL-23-mediated inflammatory pathologies.