Complement C1q and CD8+ T-cell immunity – implications for autoimmunity

Patients with the autoimmune condition systemic lupus erythematosus (SLE) develop antibodies that react with molecules found in all the cells of the body, known as autoantibodies. When autoantibodies bind to 'self' molecules, they may cause disease by inducing inflammation in the kidney, skin and other organs. A group of blood proteins called the complement system play a key role in preventing the development of SLE by facilitating the disposal of dying cells and regulating the immune response. During this award Professor Botto’s group will investigate whether and how the deficiency of one component of the complement system, C1q, alters the function of a specific type of immune cell (CD8+ T cells). Ultimately these studies will help to define a new molecular framework for addressing the role of virus infections as potential triggers of autoimmunity.