Recombinant Mouse CTLA4 protein (Fc Chimera)

補足情報

This supplementary information is collated from multiple sources and compiled automatically.

CTLA-4 also known as CD152 is an immune checkpoint receptor with a molecular weight of approximately 34 kDa. This protein is expressed on the surface of T-cells especially after activation and sometimes on regulatory T-cells (Tregs). CTLA-4 competes with CD28 for binding to the same ligands CD80 and CD86 on antigen-presenting cells. Unlike CD28 which stimulates T-cell activation CTLA-4 sends inhibitory signals to downregulate immune responses. By doing this CTLA-4 helps maintain immune system homeostasis and prevents autoimmune reactions.

Biological function summary

The CTLA-4 protein functions as a critical regulator of the immune system. It interacts with CD80/CD86 in a complex that effectively transmits inhibitory signals to T-cells. CTLA-4 controls the amplitude of the initial activation of T-cells ensuring that the body's immune responses are kept under control. In regulatory T-cells CTLA-4 engagement contributes to their immunosuppressive functions through which they maintain tolerance to self-antigens and prevent overactive immune reactions.

Pathways

CTLA-4 involves itself in the adaptive immune response pathways specifically the regulation of T-cell activity. CTLA-4's interaction with CD80/CD86 modulates pathways associated with TCR (T-cell receptor) signaling. When CTLA-4 binds its ligands it recruits phosphatases such as SHP-2 that dephosphorylate signaling proteins leading to the downregulation of T-cell interaction. This pathway interaction exemplifies how CTLA-4 acts in concert with proteins like CD28 to finely tune immune responses.

CTLA-4 plays a role in autoimmune diseases and cancer. The dysregulation of CTLA-4 function can lead to autoimmune disorders where the immune system attacks the body's own tissue. In cancer tumor cells may manipulate CTLA-4 pathways to evade immune surveillance. Targeted therapies like anti-CTLA-4 antibodies such as ipilimumab have been developed to block CTLA-4 aiming to enhance the immune system’s ability to attack cancer cells. These treatments highlight the role of CTLA-4 in balancing immune activity and the potential to alter this balance for therapeutic benefit.