Open AccessDendritic cell function in the host response to H elicobacter pylori infection of the gastric mucosa
Author(s) -
Shiu Jessica,
Blanchard Thomas G.
Publication year - 2013
Publication title -
pathogens and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.983
H-Index - 105
ISSN - 2049-632X
DOI - 10.1111/2049-632x.12014
Subject(s) - immune system , helicobacter pylori , secretion , biology , immunology , dendritic cell , gastric mucosa , proinflammatory cytokine , antigen , acquired immune system , gastritis , function (biology) , microbiology and biotechnology , inflammation , stomach , genetics , biochemistry
Dendritic cells ( DC s) 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 H elicobacter pylori ‐infected stomach is less clear. Some analyses of bone marrow‐derived DC s stimulated with H . pylori have demonstrated proinflammatory potential based on secretion of IL ‐12 or IL ‐23 or activation of T h1 and T h17 cells. Other analyses indicate that H . pylori ‐activated DC s are less responsive compared with other gastrointestinal bacteria and activate DC s to promote T reg development. DC depletion in mice supports a role for DC s in down‐regulating H . pylori ‐induced gastritis. These data indicate that gastric DC s recognize H . pylori much like DC s 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 T reg cells in the host response to H . pylori . Research is now focused on characterizing how H . pylori induces such activity in DC s and identifying the mechanisms by which H . pylori ‐activated DC s activate T reg cells.