Chapter category: Autoimmunity
Cytokines and Chemokines in Virus-Induced Autoimmunity
Cytokines and Chemokines in Autoimmune Disease
Edited by: Pere SantamariaISBN: 0-306-47693-2
» Get more information about this book at landesbioscience.com «
Chapter authors:
U Christen and M von Herrath
Virus infections usually elicit a massive inflammatory reaction characterized by release of chemokines and cytokines that attract and activate cells of the host's immune system with the goal to eliminate the foreign pathogen from the organism. In addition to the load and presentation of viral antigens, the distinct profile of chemokines and cytokines is characteristic for an individual virus infection and therefore determines the pattern of cells that infiltrate into the infected tissue or organ and the magnitude and type of the anti-viral immune response. Because viral infections induce strong cellular and humoral immune responses, their association with autoimmune diseases including type 1 diabetes, keratitis, and multiple sclerosis has been proposed and forms the basis for some animal models of autoimmune disease, such as the RIP-LCMV model for type 1 diabetes. In these experimental systems, their ability to induce diabetes,1,2 keratitis3 or allergic encephalomyelitis4 either through direct T cell cross-reactivity or cytokine/chemokine mediated 'bystander' activation of autoreactive processes has essentially been demonstrated. However, their association with human disorders has never been conclusively proven. A more recent concept proposes that the association of viral infections with autoimmunity is complex in so far as viruses can likely enhance as well as ameliorate an ongoing (for example, genetically determined) autoimmune process rather than initiating and causing all organ damage by themselves. An interesting and central question is whether and how the type of cytokine and/or chemokine profile induced by a viral infection can influence its ability to enhance or abrogate autoimmunity. In this chapter we will discuss, focused on experimental scenarios in type 1 diabetes, how this can occur, for example, by over-expression of a single cytokine, such as TNFa, or by superimposing a second viral infection on an already established auto-aggressive process. These insights should allow in the long run a better understanding of the possible pathways involved in the immunopathogenesis of human type 1 diabetes and identification of viral infections that enhance the auto-aggressive response.
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