Figure 3
Intestinal helminths trigger immune regulatory cells that can inhibit type1 diabetes and associated inflammation. Intestinal helminth infection stimulates the development of a potent type 2 immune response in the pancreatic lymph associated with decreased islet beta cell-specific interferon gamma (IFN-γ) producing Th1 cells and an increase in interleukin (IL)-4, transforming growth factor beta (TGF-β), and auto antigen-specific T cells producing IL-10. We propose that this may occur because the helminth-induced immune microenvironment in this draining lymph node alters dendritic cell (DC) activation such that these auto-antigen presenting cells now favor the development of regulatory Tr1 cells instead of inflammatory Th1 cells. We propose that this effect dampens the stimulus provided by IFN-γ that would otherwise promote the development of an inflammatory response leading to invasive insulitis and destruction of islet beta cells. It should be noted that in this context the spleen may also be an important source regulatory cell populations and cytokines.
