
The prevention and cure of common inflammatory diseases, such as arthritis, atherosclerosis, and even cancer, are controlled in part by an underlying inflammatory response. These diseases constitute increasing health problems in the 21st century with escalating costs for developed countries. Yet very few specific pharmacological agents are currently available which adequately control the development of inflammatory diseases.
Toll-like (TLR) and IL-1 receptors are members of a growing family of regulatory proteins that are central to control of immunity and inflammation. The receptors recognise a range of distinct ligands and co-receptors, but activate responses through an evolutionary conserved homologous region, the TIR domain.
The importance of TILRR as a target (as opposed to other Toll like and IL-1 receptors) is because TILRR activates the TIR domain in a distinct manner and regulates inflammatory responses and other NF-kB induced events through separate portions of the core protein, raising the possibility of being able to selectively control downstream events. TILRR has a unique combination of characteristics, including selective/distinct regulation together with a cell surface location, making TILRR a readily accessible and highly specific regulator; very desirable attributes as a target for novel therapies.
We have filed a patent application on the finding by Sheffield academics that finding that TILRR, a distinct regulator of TIR function, specifically impacts the NF-kB induced inflammatory response, thus making possible highly selective targeting.
Our patent application includes:
The research group behind this discovery are currently determining the role of TILRR in the inflammatory process and in which cell types therapeutic strategies would be most effective.
We are seeking a commercial partner to collaborate on future studies on TILRR and exploit the potential of TILRR as a drug target.