An important function of the immune system is its ability to tell between normal cells in the body and those it sees as "foreign". This allows the immune system to attack the foreign cells while leaving the normal cells alone. To do this, it uses "checkpoints". Immune checkpoints are molecules on certain immune cells that need to be activated (or inactivated) to start an immune response.
Cancer cells sometimes find ways to use these checkpoints to avoid being attacked by the immune system. But drugs that target these checkpoints hold a lot of promise as cancer treatments. These drugs are called checkpoint inhibitors.
PD-1 is a checkpoint protein on immune cells called T cells. It normally acts as a type of "off switch" that helps keep the T cells from attacking other cells in the body. It does this when it attaches to PD-L1, a protein on some normal (and cancer) cells. When PD-1 binds to PD-L1, it basically tells the T cell to leave the other cell alone.
CTLA-4 is another protein on some T cells that acts as a type of "off switch" to keep the immune system in check. Ipilimumab (Yervoy) is a monoclonal antibody that attaches to CTLA-4 and stops it from working. This can boost the body's immune response against cancer cells.
Recently, Combining immune checkpoint targeted approaches with each other or with other receptor targets is a promising schema for future therapeutic regimen designs.
Combo-RP2D by SA schedule in anti-CTLA-4 (A) and anti-PD(L)1 cohorts (B).
Humanized mice provide a system for testing how treatments modulate the human immune system, as well as create refined models for diverse infectious diseases. To assess the efficiency of new drugs as immune checkpoint inhibitors, humanized mice are required as powerful tools to help us manage or cure diseases when our own systems fail us. Genetic editing and immune reconstitution are two common approaches to humanize the mouse's immune system.
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