Figure 3

TLR-2-activated B-cells suppress Helicobacter -induced preneoplastic gastric immunopathology by inducing T regulatory-1 cells. Schematic representation of the events occurring in the course of Helicobacter-specific activation of B-cells at the site of infection (i.e. the gastric mucosa) and/or in the draining mesenteric lymph nodes. Helicobacter TLR-2 ligands activate B-cells in a MyD88-dependent manner, which leads to the expression and surface exposure of CD80, CD86 (together referred to as B7 molecules), the increased expression of CD40, and the secretion of IL-10, IL-6 and moderate amounts of TNF-α (the latter is not shown here) as well as antibodies of the IgM and IgG2b subclasses. The interaction of activated B-cells and naive T-cells induces T-cellular IL-10 expression and suppressive activity in a manner dependent on a direct interaction between both cell types via CD40/CD40L, B7/CD28 and MHCII/TCR. IL-10 secreting T-cells are essential players in the prevention of excessive Helicobacter-associated immunopathology. Adapted from [11].