Abstract

Although the majority of autoimmune diseases are under complex genetic control, environmental factors such as infections are playing an evident role in regulating autoimmunity. Studies in humans and in animal models demonstrated that infectious agents can both initiate/precipitate or prevent autoimmune disease. It has become evident that some infectious agents have evolved strategies to modulate host immune responses to facilitate survival of the pathogen while dampening down host pathology. These strategies often include modulation of cell subsets and cytokine/chemokine secretion by the host immune system. Parasitic worms like Schistosomes are master regulators of the host immune system, inducing functional and phenotypic changes in immune cells, generally inducing the expansion of Th2 responses. In the context of a Th1 or Th17 mediated autoimmune response the immunological signature induced by parasitic worms is shown to be useful to prevent of autoimmunity. The use of autoimmune disease animal models has highlighted the complex interplay between infectious agents and the host immune response. In animal models immunization with Schistosoma mansoni soluble antigen preparations can prevent experimental autoimmune encephalomyelitis (EAE), experimental colitis (EC) and protects non-obese diabetic (NOD) mice against the development of type 1 diabetes (T1D). These preparations generally induce the expansion of alternatively activated macrophages, tolerogenic DCs, iNKT cells, Th2 cells and Treg. Isolation and identification of the immunomodulatory molecules contained in such microbial extracts pave the way to the development of novel therapeutic strategies to prevent onset of T1D .