IL36B抗体—艾普蒂 新品

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     Gel: 6%SDS-PAGE, Lysate: 40 μg, Lane 1-2: PC3 cells, human fetal liver tissue, Primary antibody: P08657(PYGL Antibody) at dilution 1/300, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 30 seconds    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human thyroid cancer tissue using P08657(PYGL Antibody) at dilution 1/20. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human brain  tissue using P08657(PYGL Antibody) at dilution 1/20. (Original magnification: ×200)    

  
  

IL-36β (Interleukin-36 beta), a member of the IL-1 cytokine family, plays a key role in inflammatory and immune responses. It binds to the IL-36 receptor (IL-36R) and activates downstream signaling pathways, including NF-κB and MAPK, promoting the release of pro-inflammatory mediators. Dysregulated IL-36β signaling is implicated in inflammatory skin disorders (e.g., psoriasis), autoimmune diseases, and chronic inflammatory conditions.

IL-36β antibodies are therapeutic or research tools designed to neutralize IL-36β activity. By blocking its interaction with IL-36R, these antibodies aim to suppress excessive inflammation. In psoriasis, IL-36β overexpression correlates with disease severity, making it a promising therapeutic target. Preclinical studies show that anti-IL-36β antibodies reduce skin inflammation and cytokine production in animal models.

Currently, several monoclonal antibodies targeting IL-36 pathways are under clinical investigation, though most focus on the broader IL-36 family or its receptor. IL-36β-specific antibodies remain in earlier stages of development, with challenges including optimizing specificity and minimizing off-target effects. Their potential extends beyond dermatology to conditions like rheumatoid arthritis and inflammatory bowel disease. As research advances, IL-36β antibodies could offer tailored therapies for diseases driven by IL-36β dysregulation.