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     Black line: Control Antigen (100 ng);Purple line: Antigen (10ng); Blue line: Antigen (50 ng); Red line:Antigen (100 ng)    

  
  

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     Flow cytometric analysis of THP-1 cells using CD62P mouse mAb (green) and negative control (red).    

  
  

C4A antibodies target the C4A isoform of complement component 4 (C4), a critical protein in the classical and lectin pathways of the complement system. C4 exists as two major isoforms, C4A and C4B, encoded by highly homologous genes within the major histocompatibility complex (MHC) class III region. While both isoforms participate in pathogen clearance and immune complex processing, C4A preferentially binds amino groups, facilitating covalent attachment to immune complexes, whereas C4B reacts with hydroxyl groups, enhancing microbial opsonization.

C4A deficiency or dysfunction, often linked to gene copy number variations or mutations, is associated with autoimmune disorders, particularly systemic lupus erythematosus (SLE). Autoantibodies against C4A may arise in autoimmune contexts, potentially exacerbating complement dysregulation. These antibodies can interfere with C4A’s role in immune complex clearance, contributing to tissue inflammation and organ damage. Additionally, C4A autoantibodies have been implicated in conditions like rheumatoid arthritis and schizophrenia, though mechanisms remain under investigation.

Research on C4A antibodies focuses on their diagnostic and prognostic value. In SLE, anti-C4A antibodies correlate with disease activity and renal involvement. Their detection may aid in stratifying patients or monitoring treatment responses. However, standardization of assays and clearer pathophysiological insights are needed for clinical translation. Studies also explore genetic-epigenetic interactions influencing C4A expression and autoantibody production, offering potential therapeutic targets. Overall, C4A antibodies represent both biomarkers and mechanistic players in complement-related pathologies.