Modulation of T cell activation by the Beta2-Adrenergic Receptor

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BACKGROUND: Adaptive immune responses are coordinated by T lymphocytes, a white blood cell that circulates through blood and lymphatics of most vertebrate animals. One area that has not been widely explored is the effects of stress-activated hormones such as catecholamines, for example noradrenaline and adrenaline. T lymphocytes can sense catecholamines through a receptor called the beta2-adrenergic receptor, but how this alters adaptive immune responses is not very well understood. HYPOTHESIS AND RATIONALE: The hypothesis is that the catecholamines can either inhibit or activate T lymphocytes, depending on the types of signals from the beta2-adrenergic receptor. The first objective of this research program is to study in detail how the beta2-adrenergic receptor sends signals to T lymphocytes. The second objective of the program is to determine how catecholamines affect the ability of T lymphocytes to function in terms of their expansion and effector functions that are relevant to immunity. SIGNIFICANCE: Adaptive immune responses are necessary to fight infections, but can also cause autoimmunity, a condition where a person's own organs are attacked by the immune system. Autoimmune conditions affect millions of Canadians especially women. The link with catecholamines suggests that stress (chronic and otherwise) would affect adaptive immunity. The anticipated results we will achieve will increase our basic understanding of the immune system, and help scientists and doctors better treat infections and autoimmunity. The work also applies to maintaining healthy immunity in livestock and fish.