LILRB receptors have been shown to be upregulated in activated immune cells associated with a variety of inflammatory and autoimmune diseases. The function of the natural HLA ligands is to suppress immune cell activity through inhibitory receptor activation of SHP phosphatases and inhibition of the kinase cascades associated with immune cell activation. However, their natural function of inhibiting immune cell activity is impaired and, therefore, immune cells such as B cells, T cells and dendritic cells are activated and associated with a variety of different inflammatory diseases. ImmunOs has designed molecules that mimic the natural ligand function of HLA’s to suppress immune cell activation. The molecules either incorporate the natural native ligands or are agonistic antibodies that mimic the function of the natural ligands. These molecules are currently in non-clinical testing in a variety of assays designed to explore their activity against B, T, NK and dendritic cells as well as in primary immune cell assays.
Diagram below represent the anticipated Mechanism of Action of agonistic molecules targeting LILRB1.
NK receptors have been shown to be upregulated in activated NK cells associated with several different inflammatory diseases. While the normal function of NK inhibitory receptors is to reduce immune cell activity the natural ligands for the receptors are reduced in the inflammatory cell microenvironment. ImmunOs has designed molecules that mimic the function of the natural NK – and T-cell receptor ligands, and therefore, stimulate those cell receptor pathways that inhibit or reduce the activity of NK- and T-cells associated with autoimmunity. The NK and T cell targeting molecules have shown activity in a variety of non-clinical cell-based assays as well as pharmacodynamic activity in both ex vivo whole blood assays and in vivo models.
Diagram below represents the anticipated Mechanism of Action of natural occurring agonistic activity of HLA-E towards NKG2Awhich ImmunOs develops into an innovative anti-inflammatory treatment.
