Regulation of the immune response against infection caused by Helicobacter pylori

Abstract

The host response against H. pylori infection is ineffective in eliminating the bacteria. The innate immune system plays a central role in processing and displaying antigens from H. pylori. Regulatory cytokines (IL10 and IL12) might regulate a T-lymphocyte (Th) response type 1, leading to a chronic gastritis or a Th2 response with antibody production and bacterial erradication. IFN-g (Th1 response) might regulate the induction and expression of human leucocyte antigen-IIs (HLA-II) in epithelial cells, increasing H. pylori's adherence to the gastric epithelium and inducing apoptosis. IL-4 (Th2 response) might increase the expression of HLA-II, IgG, IgE viability and stimulation of T-cell growth. Finally recent studies are focussed on cellular apoptosis induction as a cellular growth control and as a defense response of the host to H. pylori infection.