ADO抗体—艾普蒂

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     Gel: 10%SDS-PAGE, Lysate: 30 μg, Lane: Mouse testis tissue, Primary antibody: P10646(ADO Antibody) at dilution 1/1200, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 30 minutes    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human liver cancer tissue using P10646(ADO Antibody) at dilution 1/30. (Original magnification: ×200)    

  
  

**Background of Anti-ADO Antibodies**

Anti-adenosine deaminase (ADO) antibodies target adenosine deaminase (ADA), an enzyme critical in purine metabolism. ADA catalyzes the irreversible deamination of adenosine and deoxyadenosine to inosine and deoxyinosine, preventing toxic metabolite accumulation. In humans, ADA deficiency causes severe combined immunodeficiency (SCID) due to impaired lymphocyte development and function.

ADO antibodies are primarily studied in autoimmune and inflammatory contexts. In autoimmune disorders like rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE), ADA activity may be altered, and autoantibodies against ADA have been detected, though their clinical significance remains unclear. Some studies suggest these antibodies could modulate extracellular adenosine levels, influencing immune responses or tissue inflammation.

In diagnostics, anti-ADO antibodies are not routinely measured but may serve as biomarkers in specific research settings. For example, elevated ADA levels or autoantibodies have been observed in tuberculosis pleural effusions or certain cancers, linking ADA dysregulation to disease pathology.

Therapeutic approaches targeting ADA, such as enzyme replacement or gene therapy for SCID, avoid immune responses by using polyethylene glycol-modified ADA (PEG-ADA) or patient-specific gene corrections. However, anti-ADO antibodies in non-SCID contexts remain understudied, warranting further exploration of their roles in autoimmunity, inflammation, and metabolic disorders. Challenges include standardizing detection methods and clarifying their pathogenic or protective mechanisms.