CD152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 Ramos cells using CD152 mouse mAb (green) and negative control (red).    

  
  

CD152. also known as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), is a critical immune checkpoint receptor expressed primarily on activated T cells and regulatory T cells (Tregs). Discovered in the late 1980s, it functions as a negative regulator of T-cell activation by binding to B7-1 (CD80) and B7-2 (CD86) ligands on antigen-presenting cells (APCs) with higher affinity than the co-stimulatory receptor CD28. This interaction suppresses T-cell signaling, preventing excessive immune responses and maintaining peripheral tolerance. Dysregulation of CTLA-4 is linked to autoimmune diseases and cancer.

CD152 antibodies, such as ipilimumab, were developed to block CTLA-4’s inhibitory signals, thereby enhancing T-cell-mediated anti-tumor immunity. Approved in 2011 for metastatic melanoma, ipilimumab became the first immune checkpoint inhibitor to demonstrate prolonged survival in advanced cancer. However, its use is limited by immune-related adverse events (irAEs) due to systemic immune activation. Research continues to optimize dosing, combination therapies (e.g., with PD-1/PD-L1 inhibitors), and biomarkers for patient selection. Newer anti-CD152 agents, including bispecific antibodies or those targeting specific Treg subsets, aim to improve efficacy while reducing toxicity. Understanding CD152’s dual role in immune regulation and tolerance remains central to advancing cancer immunotherapy and autoimmune disease treatments.