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Microbes and Autoimmunity

The etiology of many autoimmune diseases is considered to represent a complex interaction between genetic factors, e.g. genes encoding elements of the immune response and environmental influences. Although the molecular and cellular mechanisms by which autoimmune diseases evolve in individuals are inevitably comprised of numerous variables, there is evidence that infections may represent key elements in the development of certain autoimmune responses leading to tissue-specific destruction. Possible mechanisms by which this occurs can be generally categorized into two broad pathways consisting of antigen-specific or antigen non-specific responses. Although onset of autoimmune response may derive from one pathway, it is not impossible that both may ultimately contribute to disease. A variety of different mechanisms may contribute to the development of an autoimmune disease following microbial infection. These include (but are not limited to) molecular mimicry, presentation of autoantigen/ epitope spreading, viral/bacterial superantigens, bystander activation, and infection of lymphocytes. More importantly, these various events do not have to operate independently of one another but it is quite possible that combinations occur that contribute to disease progression. Clearly, certain microbial infections can be associated with immune responses directed against both the invading organism as well as host tissue. Yet the contribution of autoreactive lymphocytes to disease progression is sometimes not completely clear. Although animal models have provided important and valuable information with regards to mechanisms by which infection leads to autoimmune responses and enhanced and/or accelerated disease severity the relationship between infection and autoimmune disease in humans is still difficult to achieve. In addition, effective treatment of autoimmune diseases is often difficult to achieve due to various reasons including chronic antigen expression and enhanced activation of lymphocytes. This issue of Autoimmunity will focus on microbial infection and autoimmune disease. These reviews highlight key aspects with regards to induction, maintenance, and treatment of various diseases in which an autoimmune component is suspected to contribute to disease progression following infection with a virus, bacteria, or parasite. Daniel Carr (University of Oklahoma) discusses the possibility that the evolution of an autoimmune response following herpes simplex virus (HSV) infection may be dictated by both the strain of HSV as well as the genetic background of the mouse suggesting that bystander activation of lymphocytes may also contribute to tissue destruction. The relative contribution of the T cell chemokine interferon inducible protein 10 kDa (IP-10, also known as CXC chemokine ligand 10—CXCL10) to the pathology of diabetes using various elegant transgenic models and viral models of disease will be examined by Urs Christen and Matthias von Herrath (La Jolla Institute for Allergy and Immunology). Lindsay Whitton and Ralph Feuer (The Scripps Research Institute) discuss the consequences of microbial infection as it relates to the development of myocarditis and provide provocative commentary on the importance of autoreactive lymphocytes in the development and maintenance of disease. Targeting the CD40/CD154 pathway for the treatment autoimmune-induced demyelination is the subject of review provided by Laurence Howard and Stephen Miller (Northwestern University). Devin Bolz and Janis Weis (University of Utah) discusses the recent developments in host-pathogen interactions resulting in arthritis following infection with Borrelia burgdorferi. Finally, Desnise Golgher and Ricardo Gazzinelli (Federal University of Mina Gerais) provides a succinct