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     The image is immunohistochemistry of paraffin-embedded Human lung cancer tissue using P00130(IL23R Antibody) at dilution 1/10. (Original magnification: ×200)    

  
  

The IL-23 receptor (IL23R) is a key component of the IL-23 signaling pathway, which plays a pivotal role in mediating inflammatory and autoimmune responses. IL-23. a cytokine belonging to the IL-12 family, binds to IL23R—a heterodimeric receptor complex composed of IL23R and IL-12Rβ1 subunits. This interaction activates the JAK-STAT pathway, particularly STAT3. driving the differentiation and maintenance of Th17 cells, which produce pro-inflammatory cytokines like IL-17 and IL-22. Dysregulation of this pathway is implicated in chronic inflammatory diseases, including psoriasis, inflammatory bowel disease (IBD), and ankylosing spondylitis.

IL23R-targeted antibodies are biologic therapies designed to disrupt IL-23 signaling, thereby reducing pathogenic inflammation. These monoclonal antibodies either bind directly to the IL-23p19 subunit (e.g., risankizumab, guselkumab) or block IL-23’s interaction with its receptor (e.g., tildrakizumab). By selectively inhibiting IL-23. these agents suppress Th17 cell activation and downstream cytokine production without broadly impairing immune function. Clinical trials have demonstrated their efficacy in inducing and sustaining remission in conditions like moderate-to-severe plaque psoriasis and Crohn’s disease, often with favorable safety profiles compared to older biologics. Research continues to explore their potential in other IL-23/Th17-driven disorders, highlighting IL23R as a critical therapeutic target in precision immunology.