BTLA抗体

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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 Hela cells using BTLA mouse mAb (green) and negative control (red).    

  
  

BTLA (B and T Lymphocyte Attenuator) is an inhibitory immune checkpoint receptor predominantly expressed on B cells, T cells, and dendritic cells. Belonging to the CD28 receptor family, BTLA regulates immune activation by delivering co-inhibitory signals upon binding to its ligand, herpesvirus entry mediator (HVEM). The BTLA-HVEM interaction plays a dual role in immune modulation: HVEM can either suppress T-cell responses via BTLA engagement or promote pro-inflammatory signals by binding to other receptors like LIGHT. This balance is critical for maintaining immune homeostasis and preventing excessive inflammation or autoimmunity.

BTLA gained attention as a potential therapeutic target in cancer immunotherapy due to its role in dampening antitumor immunity. Antibodies targeting BTLA aim to block its inhibitory signaling, thereby revitalizing exhausted T cells and enhancing tumor clearance. Preclinical studies show that anti-BTLA antibodies, alone or combined with PD-1/PD-L1 inhibitors, improve antitumor responses in murine models. Conversely, agonist anti-BTLA antibodies are explored for treating autoimmune diseases by amplifying inhibitory signals to curb overactive immune cells.

Despite promising preclinical data, clinical translation remains in early stages. Phase I trials of anti-BTLA antibodies (e.g., icibrutimab) demonstrate manageable safety profiles and preliminary efficacy in advanced solid tumors. Challenges include optimizing targeting strategies and understanding context-dependent BTLA functions across immune cell subsets. Further research is needed to unravel its complex biology and therapeutic potential in immune-related disorders.