Dual Role of CXCL10 as Conductor of Cellular Trafficking during Type 1 Diabetes

One possible way of how autoimmune disease can be initiated is by infection with a foreign pathogen. Especially viruses are thought to act as triggering factors, inducing a detrimental attack against ‘self’ by the immune system of a susceptible host because of two major reasons. First, viruses cause a massive inflammation of the infected tissue and therefore initiate the infiltration of a broad variety of leukocytes, including potentially ‘self’-reactive lymphocytes. Second, some viruses have been demonstrated to bear molecules with a strong structural similarity to host components. The existence of such a ‘molecular mimicry’ may elicit an immune response, which is initially generated in defense against the invading pathogen but in a second wave targets similar structures of the host. In the present review we will reflect on the dual role of inflammatory factors during this process and discuss possibilities of how such a detrimental second wave of the immune system can be blocked. Most of the presented data have been obtained from animal models that integrate the concept of molecular mimicry. They use transgenic mice expressing a defined model protein specifically in a target tissue and a virus containing either an identical or a similar protein as a triggering factor.