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

  
  

Glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR), also known as TNFRSF18. is a cell surface receptor belonging to the TNF receptor superfamily. Primarily expressed on regulatory T cells (Tregs) and activated effector T cells, GITR plays a dual role in immune regulation. Its interaction with its ligand (GITRL) enhances effector T cell activation, proliferation, and cytokine production, while simultaneously suppressing the immunosuppressive function of Tregs. This unique mechanism positions GITR as a promising therapeutic target for modulating antitumor immunity and autoimmune diseases.

GITR-targeting antibodies, typically designed as agonistic agents, aim to amplify antitumor responses by boosting effector T cell activity and overcoming Treg-mediated immune suppression. Preclinical studies in cancer models demonstrate that GITR agonism promotes tumor regression, often synergizing with checkpoint inhibitors like anti-PD-1/PD-L1 therapies. However, clinical trials have shown mixed results, with efficacy influenced by antibody design, dosing strategies, and patient selection. Some candidates, such as INCAGN01876 and MK-4166. have progressed to phase I/II trials, highlighting both safety profiles and variable tumor response rates. Challenges remain in optimizing target engagement and minimizing systemic immune-related adverse events. Current research focuses on combination therapies, biomarker identification, and engineering bispecific antibodies to enhance tumor-specific targeting.