Atherosclerosis is a multifactorial disease, but an unbalanced immune system plays a critical role in the disease development. A common theory states that a continuous stress to the vascular vessel wall initiates a repair process that however is insufficient to completely heal the tissue. This imbalance is associated with accumulation of cholesterol, which is an essential component of cellular membranes, and inflammatory cells at the injury site. Since cholesterol particles are not normally accumulating extra-cellularly, they are affected by the inflammatory environment, which modifies the particle structure. Since this can be potentially dangerous an inflammatory response is initiated in order to remove the modified particles. However, the continuous stress leads to an imbalanced immune response, which aggravate the inflammation and leads to a larger wound. In this thesis I present two methods on how to balance the immune response in order to stabilize the wound and thereby reduce the risk of rupture. I also elucidate the role of CD8+ T lymphocytes in the development of atherosclerotic lesions and test the association between CD8+ T lymphocytes in blood and cardiovascular disease.

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