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.
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 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 interleukin-23 receptor (IL-23R) gene plays an important role in the progression of inflammatory and autoimmune diseases and IL-23 polymorphisms might influence the susceptibility of pre-eclampsia.
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.
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.
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.
Therefore, AS2762900-00 represents a potent novel IL-23-IL-17 pathway inhibitor with the potential to be developed into a new therapy for the treatment of autoimmune diseases.
Previous studies have explicitly shown that psoriasis is an autoimmune disease that is predominantly mediated by T helper 17 (Th17) cells, which express high levels of interleukin-17 (IL-17) in response to interleukin-23 (IL-23).
IL-23 binds IL-23R on the surface of target cells and transmits signals through Janus kinase 2/signal transducer and activator of transcription channels, participating in the occurrence of chronic inflammatory diseases and autoimmune diseases.
Nevertheless, biological drugs that target the IL-23-IL-17 pathway are highly effective in treating human psoriasis and are showing promise in the treatment of relapsing remitting MS and other T-cell mediated autoimmune diseases.
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.
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.
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.
The selective requirement of JunB for IL-23-dependent T<sub>H</sub>17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases.
To further dissect the role of IL-23 in the expression of autoimmunity and related pathology, we generated IL-23 receptor-deficient MRL.<i>lpr</i> mice.