The cytokines interleukin (IL)-12 and IL-23 are heterodimeric proteins containing two subunits: the p40 subunit is common to both cytokines; p35 and p19 subunits are present in IL-12 and IL-23, respectively (Coskun et al., 2017; Currò et al., 2017). IL-12 and IL-23 are both induced as part of the innate immune response in patients with IBD (Neurath, 2017). Indeed, these are among the main cytokines arising as a consequence of this (Argollo et al., 2017).
IL-12 and IL-23 can both produce pro-inflammatory responses via JAK signalling (Coskun et al., 2017); IL-23 may also act via the IL-17 and interferon gamma pathways (Argollo et al., 2017). However, their main effect arises through their induction of T helper (Th) cells (Coskun et al., 2017). IL-12 induces differentiation of Th1 cells and IL-23 induces differentiation of Th17 resulting in increased production of inflammatory cytokines (Coskun et al., 2017; Currò et al., 2017).
Video 1. Animation of the IL-12 and 1L-23 Th cell pathways (Coskun et al., 2017).
Mucosal Th1 responses have been found in Crohn’s disease, while Th17 responses are apparent in both Crohn’s disease and ulcerative colitis (Neurath, 2017). Given the actions of IL-12 and IL-23, blocking the activity of these cytokines may be a therapeutic option for patients with IBD (Argollo et al., 2017; Coskun et al., 2017; Neurath, 2017).
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