Immune cells carry surface proteins that act like a set of brakes and accelerators, and this project will map the molecular structure of one fast-evolving family of these control switches. The proteins, called paired receptors, have nearly identical external sections that recognise other cells but send completely opposite signals—some activate an immune response, others shut it down. Researchers suspect that bacteria and viruses may have evolved to grab these receptors directly, hijacking the body’s ability to calibrate its defence. Without a clear molecular picture of how these receptors bind and signal, it is impossible to design drugs that either block or enhance their effect. This is fundamental science: the work will use quantitative analysis to identify the precise parameters that determine whether a receptor triggers attack or tolerance. If successful, it will provide a mechanistic understanding that could inform future therapies for cancer, infectious diseases, and autoimmune conditions such as arthritis and diabetes, where the immune system’s volume control has gone wrong.
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The immune system is remarkable in that it can recognise foreign materials such as bacteria and viruses without having encountered them before and make a measured response that leads to their elimination. It can distinguish between small infections at the site of, for example a bite, from a viral infection like influenza that calls for all the power of the immune system to be mobilised. This control is mediated by white blood cells patrolling the body waiting to react. The nature of the responses is highly controlled and this involves interactions of proteins at the surface of the blood cells with other cells. This proposal looks at one class of proteins called paired receptors that have been implicated in virus defence and have the intriguing property that they can give very different signals although the bit that recognises other cells is quite similar. These paired receptors are evolving very fast and the hypothesis is that bacteria and viruses might bind them directly and therefore affect responses to them and also the immune system in general. The aim is to understand the mechanisms involved at a molecular level for this interaction. The use of quantitative molecular analysis in this study will identify parameters involved in determining the signal produced with relevance for therapies involving this type of target and for the general understanding of the immune system. Thus it will have implications in understanding and treating diseases like cancer, infectious diseases and autoimmune disease such as arthritis, diabetes.
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