LILRB2抗体—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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     Western blot analysis using LILRB2 mouse mAb against MOLT4 (1) and K562 (2) cell lysate.    

  
  

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     Flow cytometric analysis of HL-60 cells using LILRB2 mouse mAb (green) and negative control (red).    

  
  

LILRB2 (Leukocyte Immunoglobulin-Like Receptor B2), a member of the inhibitory LILR family, is an immune checkpoint receptor expressed on myeloid cells, such as macrophages, dendritic cells, and neutrophils, as well as subsets of lymphocytes. It binds to MHC class I molecules and other ligands, transmitting inhibitory signals through immunoreceptor tyrosine-based inhibitory motifs (ITIMs) to dampen immune activation. In physiological conditions, LILRB2 helps maintain immune tolerance and prevent excessive inflammation. However, in cancer, LILRB2 is exploited by tumors to evade immune surveillance. Tumor cells often overexpress MHC class I-related molecules (e.g., HLA-G) that engage LILRB2. suppressing antigen presentation, inhibiting pro-inflammatory cytokine production, and promoting an immunosuppressive microenvironment.

LILRB2-targeting antibodies are being developed to block this interaction, aiming to reverse immune suppression and enhance anti-tumor responses. Preclinical studies show that anti-LILRB2 antibodies can reprogram myeloid cells toward a pro-inflammatory phenotype, boost T-cell activity, and synergize with PD-1/PD-L1 inhibitors. Challenges include optimizing specificity to avoid off-target effects and understanding context-dependent signaling, as LILRB2 may have dual roles in different immune cell types. These antibodies represent a promising strategy in cancer immunotherapy, particularly for MHC class I-high tumors resistant to existing checkpoint therapies.