In this regard, immunogenic DCs produce IL-12 and IL-23 favouring the acquisition of Th1 and Th17 inflammatory phenotypes, respectively, by autoreactive CD4<sup>+</sup> T-cells, thus promoting autoimmunity.
IL-23/Th17 pathway has been identified to sustain inflammatory condition in several autoimmune diseases and therefore being targeted in various therapeutic and effective approaches.
IL-23/Th17 signaling pathway plays a crucial role in the cell-mediated immune response against bacterial infections and also in the pathogenesis of inflammatory and autoimmune diseases.
An overview of the emerging role of IL-23 in physiological and pathological conditions and a review of the different approaches (IL-23 pathway-based) currently used for autoimmune diseases and cancer therapies and the results obtained both in preclinical models and in clinical trials.
Interleukin-23 (IL-23) has been implicated in inflammatory and autoimmune diseases by skewing CD4<sup>+</sup> T helper cells towards a pathogenic Th17 phenotype.
We propose that IL-23 promotes the development of lupus-like autoimmunity not only through T cell polarization and cytokine production in the peripheral lymphoid organs but also by influencing T cell thymic development.
IL-23/STAT3 signaling pathway is a key process in Th17 cell differentiation, and Th17 cells are closely related to the development of autoimmune diseases.
Since the IL-23/IL-17 pathway is known to associate with other autoimmune diseases, including rheumatoid arthritis (RA) and systemic sclerosis (SSc), we hypothesised that IL-23R could be a shared susceptibility gene.
The subunit of IL-23 (IL12B) and its receptor (IL23R) gene single-nucleotide polymorphisms (SNPs) have been shown to be associated with several autoimmune diseases such as inflammatory bowel disease, psoriasis and ankylosing spondylitis.
The nucleotide polymorphism in the promoter region of <i>Il12b</i> (rs41292470 consisting of the long or short allele) encoding the shared subunit of IL-12 and IL-23, p40, has been reported to associate with susceptibility to infectious diseases and autoimmune disorders.
In conclusion, simultaneous knock-down of CD40 and IL-23 production by BMDCs may represent a promising therapeutic tool for the treatment of IL-17-dependent autoimmune diseases, including multiple sclerosis.
IL-23 is the key cytokine for generation of pathogenic IL-17-producing helper T (T<sub>H</sub>17) cells, which contribute critically to autoimmune diseases.
The results showed that the transducted hAD-MSCs/RIL-23R, expressing IL-23 decoy receptor, can provide a useful approach for a basic research on cell-based gene therapy for autoimmune disorders.
Molecular characterization of the binding epitope of IL-23R and its cognate cytokine IL-23 is paramount to understand the role in autoimmune diseases and to support the discovery of new inhibitors of this protein-protein interaction.
Because microglia produce IL-1beta and IL-23, these cytokines may act in an autocrine manner to induce IL-17 expression in microglia, and thereby contribute to autoimmune diseases, such as MS, in the central nervous system.
IL-23, which is composed of p19 and p40 subunits, is a proinflammatory cytokine that contributes to the formation and maintenance of Th17 cells in inflammatory autoimmune diseases.