IL-23, which is mainly secreted by antigen-presenting cells, is a member of the IL-12 family, which includes IL-12, IL-27, and IL-35. IL-23 is a heterodimeric cytokine, comprised of a unique p19 subunit and p4 subunit, the latter of which is shared with IL-12. The receptor for IL-23 consists of IL-23R and IL-12Rβ1, the latter of which is also characteristic of IL-12. IL-23 is essential for Th17 differentiation, expansion, and survival by binding to its receptor, thereby activating the signaling pathway. Many studies revealed that the IL-23/Th17 pathway is implicated in the pathophysiology of various autoimmune diseases, such as autoimmune arthritis, primary biliary cirrhosis, and inflammatory bowel disease.
Interleukin 23 (IL-23) is a heterodimeric cytokine composed of two disulfide-linked subunits, a p19 subunit that is unique to IL-23, and a p40 subunit that is shared with IL-12. The p19 subunit has homology to the p35 subunit of IL-12, as well as to other single chain cytokines such as IL-6 and IL-11. The p40 subunit is homologous to the extracellular domains of the hematopoietic cytokine receptors. Although p19 is expressed by activated macrophages, dendritic cells, T cells, and endothelial cells, only activated macrophages and dendritic cells express p40 concurrently to produce IL-23. IL-23 has biological activities that are similar to, but distinct from IL-12. Both IL-12 and IL-23 induce proliferation and IFN-gamma production by human T cells. While IL-12 acts on both naive and memory human T cells, the effects of IL-23 is restricted to memory T cells.
Interleukin 23 receptor (IL23R), a heterodimer of the IL12 receptor β1 (IL12Rβ1) and IL12Rβ2, is a type I cytokine receptor for IL23. IL23R is comprised of two subunits, the IL12Rβ1 subunit, which is shared with several cytokines, and a subunit that is unique to IL-23. IL23, after binding to IL23R, activates memory T cells and mediates pro-inflammatory activities in part by the production of IL17 through activation of TH17 lymphocytes. IL23R is expressed on T cells, NK cells, dendritic cells, and macrophages. In fact, polymorphisms of the IL23R gene were reported to be associated with susceptibility to inflammatory diseases and autoimmune diseases such as psoriasis, multiple sclerosis, Graves's ophtalmopathy and inflammatory bowel diseases. The IL23R is known to be critically involved in the carcinogenesis of different malignant tumor.
Multifunctional cytokine mainly produced by T-cells that plays a regulatory role in immune response, tissue homeostasis, host defense, and oncogenesis. Possesses antiviral functions and induces the type I intereferon response during influenza infection. Signals through two receptor complexes IL20RA/IL20RB or IL20RB/IL22RA1. In turn, stimulates the JAK1-STAT3 and MAPK pathways and promotes the secretion of pro-inflammatory mediators including IL8 and MMP1. Intracellularly, maintains endoplasmic reticulum homeostasis by restricting the eIF2alpha-CHOP pathway-mediated stress signal. In addition, acts as a quality control mechanism for the ubiquitin proteasome system by alerting the cell to proteasome dysfunction through activation of PKR/EIF2AK2.
Interleukin-25 (IL-25) is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. IL-25 is a member of the IL-17 family of cytokines. However, unlike the other members of this family, IL-25 promotes T helper (Th) 2 responses. IL-25 also regulates the development of autoimmune inflammation mediated by IL-17–producing T cells. IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin (TSLP)–activated dendritic cells (DCs), homeostatic cytokines, or T cell receptor for antigen triggering. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. A plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells had been provided.
Possesses antiviral functions and induces the type I intereferon response during influenza infection. Signals through two receptor complexes IL20RA/IL20RB or IL20RB/IL22RA1. In turn, stimulates the JAK1-STAT3 and MAPK pathways and promotes the secretion of pro-inflammatory mediators including IL8 and MMP1 (By similarity).
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