The immune system has evolved complex mechanisms that allow rapid and destructive responses to microbial intruders while sparing the host’s own tissues. Regulation of this delicate balance depends mainly on the immune system’s two major types of T cell, which are distinguished by the protein — either CD4 or CD8 — that is expressed on their surface. They are called CD4 T cells and CD8 T cells, respectively. The task of CD8 T cells has generally been assumed to be to kill cells infected with microbial invaders and to destroy foreign or abnormal cells. However, writing in Nature, Saligrama et al.1 report another role: CD8 T cells can inhibit self-reactive CD4 T cells and quell autoimmune disease in a mouse model of multiple sclerosis.
In previous work2, researchers from the present group showed that, if people with coeliac disease were exposed to gluten proteins (a major type of trigger, called an allergen, in this autoimmune disorder), it activated not only CD4 T cells that could specifically recognize gluten, as expected, but also a subset of CD8 T cells. Exactly what the latter were doing, however, was unclear. Saligrama and colleagues now report their investigation into whether a similarly coordinated T-cell response might be detected in experimental autoimmune encephalomyelitis (EAE), which is a mouse model of multiple sclerosis. This autoimmune model can be induced by injecting the protein myelin oligodendrocyte glycoprotein (MOG), a component of the fatty coating of nerve cells called myelin, into mice. The authors identified populations of both CD4 and CD8 T cells (among other immune cells) that proliferated vigorously after immunization with MOG, generating clones of cells…
