Humanized Immune Checkpoint (ICP) Mouse Models
Therapies targeting immune checkpoints (ICPs) are changing the practice of medical oncology. genOway has developed a catalog of reliable and efficient translational mouse models for immunotherapy expressing humanized immune checkpoints.
These models are suitable to assess the efficacy of compounds targeting immune checkpoints in fully immunocompetent mice. Moreover, they represent a powerful model system for studying how compounds modulate immune cell response and/or stroma cells in a physiological microenvironment.
- Physiological expression of the human target(s)
- Preservation of the target-ligand interaction
- Fully functional mouse immune system
- Lack of expression of the murine target gene thus avoiding cross-reactivity
Suitable for studying:
- Well-calibrated syngeneic tumor models
- Long-term treatment(s)
- T cell exhaustion and reminiscence
VISTA (V-domain Ig suppressor of T cell activation) is a type 1 transmembrane protein produced at high levels in tumor-infiltrating lymphocytes (TILs).
PD-1 (programmed cell death protein 1) is a cell surface protein that down-regulates the immune system, thus preventing autoimmune diseases but also cancer cell eradication.
OX-40, also known as TNFRSF4 (tumor necrosis factor receptor superfamily member 4), is a secondary co-stimulatory immune checkpoint molecule that plays a key role in the development of several autoimmune and inflammatory diseases.
GITR (glucocorticoid-induced tumor necrosis factor receptor-related protein), also known as TNFRSF18 (tumor necrosis factor receptor superfamily member 18), is a co-stimulatory immune checkpoint molecule that has been shown to be involved in programmed cell death and dominant immunological self-tolerance maintained by CD25+/CD4+ regulatory T cells.
CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), also known as CD152 (cluster of differentiation 152), is an immune checkpoint that acts as a negative regulator of T cell activation, thereby down-regulating the immune response.