Along with other NKRs, LLT1/CD161 interaction seems to fine-tune the responsiveness of NK cells, downmodulating effector responses and being involved in NK cell peripheral self-tolerance, independently of MHC class I. If LLT1 is viewed as a self-ligand not expressed under resting conditions and upregulated upon activation, the level of expression of CD161 also appears to be modulated by infection and inflammation. This evidence concerns the gene KLRB1 and infection.