Infection by the
gastroduodenal pathogen Helicobacter pylori elicits a complex immunologic response in the
mucosa involving
neutrophils,
plasma cells,
eosinophils, and
lymphocytes, of which
T cells are the principal orchestrators of immunity. While so-called classical
T cells (e.g.
T-helper cells) that are activated by
peptide fragments presented on
antigen-presenting cells have received much attention in
H. pylori infection, there exists a diverse array of other
T cell populations that are potentially important for the outcome of the ensuing
immune response, some of which have not been extensively studied in
H. pylori infection. Pathogen-specific
regulatory T cells that control and prevent the development of
immunopathology associated with
H. pylori infection have been investigated, but these cells can also benefit the
bacterium in helping to prolong the
chronicity of the
infection by suppressing protective
immune responses. An overlooked
T cell population, the more recently described
Th17 cells, may play a role in H. pylori-induced
inflammation, due to
triggering responses that ultimately lead to the recruitment of polymorphs, including
neutrophils. The so-called innate or unconventional
T cells, that include two conserved
T cell subsets expressing invariant antigen-specific receptors, the CD1d-restricted
natural killer T cells which are activated by
glycolipids, and the mucosal-associated invariant
T cells which play a role in defense against orally
acquired pathogens in the
intestinal mucosa, have only begun to receive attention. A greater knowledge of the range of
T cell responses induced by
H. pylori is required for a deeper understanding of the
pathogenesis of this
bacterium and its ability to perpetuate chronic
infection, and could reveal new strategies for therapeutic exploitation.
