Molecular mechanisms of the GIMAP-5-dependant cell survival pathway in T lymphocytes

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A subset of white blood cells called as 'T cells' are very important to safeguard us from infectious agents such as bacteria and viruses. Under certain circumstances these cells become activated and kill normal tissues leading to autoimmune diseases such as type 1 diabetes and multiple sclerosis. The circulating T lymphocytes survive for long periods of time. Their survival depends on several factors. One of them is a protein called as GIMAP5. In one particular strain of rat called the BB-DP rat the protein GIMAP5 is defective. As a consequence, the T cells in these rats die spontaneously. Therefore these rats cannot protect themselves from infections. GIMAP5 was discovered in 2002 and nothing much is known about its structure or functions. With funding from NSERC, my group showed that GIMAP5 does not function like classical proteins that are involved in cell survival. In this renewal project, I will identify the molecules with which GIMAP5 interacts, understand the mechanisms by which GIMAP5 mediates its survival functions and correlate the function with different part of GIMAP5 protein. Proteins with similar structure are also present in the plants. These proteins protect the plants from certain pathogens. The current project will help in understanding how GIMAP5 and other similar proteins that belong to the family of GIMAP mediate their functions.