Dendritic cell function in the host response to Helicobacter pylori infection of the gastric mucosa

Authors


  • This MiniReview concisely summarizes the evidence that dendritic cells play an important role in modulating T cell responses to Helicobacter pylori infection, primarily through the development of regulatory T (Treg) cells, which may limit the gastritis associated with this infection.

Abstract

Dendritic cells (DCs) play an important role as antigen-presenting cells that direct the nature of the adaptive immune response. Subtypes are differentiated by lineage, tissue, marker expression and function. Their function in promoting regulatory T cells in the gut to maintain immunologic homeostasis is well documented, but their role in the Helicobacter pylori-infected stomach is less clear. Some analyses of bone marrow-derived DCs stimulated with H. pylori have demonstrated proinflammatory potential based on secretion of IL-12 or IL-23 or activation of Th1 and Th17 cells. Other analyses indicate that H. pylori-activated DCs are less responsive compared with other gastrointestinal bacteria and activate DCs to promote Treg development. DC depletion in mice supports a role for DCs in down-regulating H. pylori-induced gastritis. These data indicate that gastric DCs recognize H. pylori much like DCs in the gut that recognize commensal organisms and promote a regulatory T-cell response. This is consistent with a growing body of literature documenting the prevalence and function of Treg cells in the host response to H. pylori. Research is now focused on characterizing how H. pylori induces such activity in DCs and identifying the mechanisms by which H. pylori-activated DCs activate Treg cells.

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