Special Contribution Helminth Infections Prevent Autoimmune Diseases through Th2-Type Immune Response

Helminth parasites are known to elicit the immune response towards T helper 2 (Th2)type, characterized by Th2 related cytokines, that typically include interleukin-4 (IL4), IL-5 and IL-13. In this review we will describe the mechanisms involved in helminth induced Th2 immune response. Intestinal epithelial cells (IECs) produce thymic stromal lymphopoietin (TSLP), which is both necessary and sufficient for the initiation of Th2 cytokine-driven inflammation. IL-33 mRNA is expressed early during parasite infection and IL-33 binds ST2 receptor, both of which are associated with optimal CD4+ Th2 polarization. Following innate immune cell recognition, basophils and mast cell can secrete Th2 type cytokines that are thought to contribute to CD4+ Th2 differentiation. Additionaly, dendritic cell conditioned with some helminth products can promote CD4+ Th2 differentiation. Alternatively activated macrophages, activated by the Th2 cytokines IL-4 and IL13 in parasitic infections, contribute to the host protective response: control of Th1-type inflammation, wound healing and worm expulsion. Experimentally, helminths have been associated with protection against a number of autoimmune disorders, including inflammatory bowel diseases and type 1 diabetes. It may be a novel strategy to ameliorate autoimmune inflammation by expanding and activating the Th2 response originated from parasites.