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The immune system protects us from harmful invaders like bacteria, viruses, and parasites, and also removes cancer cells. To keep us healthy, it needs to stay in balance. If it works too hard, it can cause autoimmune diseases, but if it’s too weak, we might become more vulnerable for infections and cancer.

Special proteins called immune inhibitory receptors (IIRs) help keep this balance. They act like brakes on the immune system, stopping it from becoming overactive. Some cancers use these brakes to hide from immune cells. Cancer treatments can block IIRs so the immune system can attack again. In diseases where the immune system is too active, turning on IIRs can help calm it down.

In this thesis we studied three IIRs, CD200R, PD-1, and LAIR-1. 
•    For CD200R, we found specific regions that are needed for it to slow down immune activity and discovered a new pattern that CD200R uses to send its inhibitory signals. 
•    For PD-1, which is an important target in cancer therapy, we showed that certain inflammatory substances can make PD-1 treatment less effective in the lab. 
•    For LAIR-1, we studied the interaction with another IIR, LILRB4. We found that LAIR-1 likely disrupts the function of LILRB4, when LAIR-1 and LILRB4 are both on the same cell.

In summary, our research contributed to the understanding of IIRs. Context, like inflammation and the presence of other IIRs, can influence IIRs. This knowledge can help improve future treatments for cancer, autoimmune diseases, and infections.