Immune Modulation by Schistosoma mansoni Infection and its Implication in Auto Immune Disorders and Allergic Diseases

Abstract

The immune response during the acute phase of schistosoma mansoini infection is associated with type 1 helper T-cells (Th1) response with increased production of tumor necrosis factor (TNF-α) and interferon-γ (IFN-γ) while in chronic phase the immune response is associated with type 2 helper T-cells (Th2) type, with elevated levels of interleukin (IL)-4, IL-5, and IL-10 and decreased levels of IFN-γ. This down modulation is mediated by S. mansoni antigen driven IL-10 production. IL-10 modulates the expression of co-stimulatory molecules and the production of pro-inflammatory cytokines such as IFN-γ, TNF-α by acting on macrophages. IL-10 also inhibits the differentiation of dendritic cells and suppresses the production of Th1 and Th2 type chemokines and cytokines. Evidence indicates chronic exposure to S. mansoni to down regulate the type 1 immune response and prevents the onset of Th1 mediated diseases such as multiple sclerosis, diabetes mellitus and Cronh’s diseases. Furthermore, chronic exposure to S. mansoni also down regulate Th2 mediated diseases such as atopic asthma and allergic rhinitis. This is mainly associated with diminished IL-5 production and increased IL-10 production by peripheral blood mononuclear cells in response to the parasite antigens. IL-10 induced by the parasite antigen interferes with allergic effector mechanisms either by inhibiting mast cell degranulation or by inhibiting Th2 cell proliferation. Generally, it seems that S. mansoni infection could mediate protection against allergic diseases and auto immune disorders. Identification of parasite molecules that induce protection and the way in which the parasite modulates immune response is critical to discover safe and effective drugs for the treatment of chronic inflammatory and allergic diseases.