GPI抗体—艾普蒂

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     Gel: 8%SDS-PAGE, Lysate: 40 μg, Lane 1-5: PC3, Raji, Hela, 231 and Jurkat cell lysates, Primary antibody: P06571(GPI Antibody) at dilution 1/1000, Secondary antibody: Goat anti rabbit IgG at 1/5000 dilution, Exposure time: 3 minutes    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human esophagus cancer using P06571(GPI Antibody) at dilution 1/45. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human gastric cancer using P06571(GPI Antibody) at dilution 1/45. (Original magnification: ×200)    

  
  

**Background of GPI Antibodies**

Glucose-6-phosphate isomerase (GPI) is a ubiquitously expressed enzyme that catalyzes the interconversion of glucose-6-phosphate and fructose-6-phosphate in glycolysis. Beyond its metabolic role, GPI has gained attention as an autoantigen in autoimmune diseases, particularly rheumatoid arthritis (RA). Anti-GPI antibodies were first identified in the K/BxN mouse model of RA, where they trigger severe joint inflammation by forming immune complexes that activate complement and recruit inflammatory cells.

In humans, elevated anti-GPI antibodies are detected in a subset of RA patients, correlating with disease severity and joint damage. These antibodies may contribute to pathogenesis by binding synovial GPI, promoting cytokine release, and enhancing osteoclast-mediated bone erosion. However, their diagnostic specificity remains limited, as they are also found in other conditions like lupus and infections.

Research on GPI antibodies highlights the interplay between metabolic enzymes and autoimmunity, suggesting that post-translational modifications or abnormal exposure of GPI in stressed cells might break immune tolerance. Current studies focus on their role as biomarkers and therapeutic targets, though clinical applications require further validation. Understanding GPI antibody dynamics offers insights into RA mechanisms and broader autoimmune pathways.