Grant: CIHR Fellowship

Multiple sclerosis (MS) affects more than 2 million people worldwide and has a severe impact on their quality of life. MS involves an abnormal response of the body's immune system which is directed against the brain. In MS patients, an abnormal immune cell infiltration across blood vessels occurs, enabling harmful cells to enter the brain where they start attacking myelin, the protective sheath surrounding nerve cells. To enter the brain, immune cells use so-called "adhesion molecules". In this project, I aim to restrict this immune cell infiltration by blocking a novel adhesion molecule called "adipocyte adhesion molecule" (or ACAM). ACAM was originally characterized in fat cells and was found to be critically involved in the development of obesity. To date, the possible implication of ACAM in inflammatory processes or MS has not yet been studied. Nevertheless, my own preliminary findings show that ACAM is expressed on both immune cells and on blood vessels of the brain, both in humans and in mice, especially during inflammatory processes. Indeed, I showed that there is an abnormal increase of the quantity of ACAM on vessels and immune cells in active MS lesions. Furthermore, ACAM expression is also increased in animal models of MS. Therefore, my hypothesis is that ACAM plays a critical role in MS by promoting the migration of disease-causing immune cells across blood vessels of the brain. I aim to unravel how ACAM plays a role in immune cell entry into the brain and establish the therapeutic potential of blocking ACAM in preventing MS development and/or progression.