CD32B抗体;CD32B Antibody—艾普蒂

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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 Jurkat cells using CD32B mouse mAb (green) and negative control (red).    

  
  

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     Flow cytometric analysis of THP-1 cells using CD32B mouse mAb (green) and negative control (red).    

  
  

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     Flow cytometric analysis of K562 cells using CD32B mouse mAb (green) and negative control (red).    

  
  

CD32B (also known as FcγRIIB) is a member of the Fc gamma receptor family, primarily expressed on B cells, dendritic cells, macrophages, and other immune cells. As the sole inhibitory Fcγ receptor in humans, it contains an immunoreceptor tyrosine-based inhibitory motif (ITIM) in its cytoplasmic domain, enabling it to suppress immune activation signals. CD32B binds the Fc region of IgG immune complexes, modulating immune responses by balancing activating signals from other Fc receptors (e.g., FcγRI, FcγRIIA, FcγRIII). This regulation is critical for preventing hyperactivation in autoimmune diseases and maintaining immune tolerance.

Therapeutically, CD32B has gained attention as a target in autoimmune disorders and cancer. In autoimmunity, enhancing CD32B signaling may dampen pathogenic antibody-driven inflammation. Conversely, in oncology, blocking CD32B on tumor-associated macrophages or B cells can enhance the efficacy of monoclonal antibody therapies (e.g., rituximab) by preventing inhibitory signaling that compromises antibody-dependent cellular cytotoxicity (ADCC) or phagocytosis. Recent studies also explore its role in modulating checkpoint inhibitor responses.

Despite its potential, targeting CD32B remains challenging due to its overlapping expression with activating receptors and the need for cell-specific modulation. Ongoing research focuses on developing agonistic/antagonistic antibodies or engineered Fc domains to fine-tune CD32B activity, aiming to optimize therapeutic outcomes while minimizing off-target effects.