Abstract
Helicobacter pylori is one of the most common human pathogens and is associated with chronic gastritis, peptic ulcers and gastric carcinoma. H. pylori establishes a persistent infection, suggesting that the host response is ineffective in clearing the infection. H. pylori employs multiple mechanisms to undermine host responses. For example, CD4+ T cells are recruited to the gastric mucosa of infected individuals, but these cells are predominantly T helper 1 (TH1) cells, which do not provide protection from the extracellular pathogen. H. pylori neutrophil-activating protein (HP-NAP) promotes the TH1 polarized response. HP-NAP induces macrophages and dendritic cells to produce IL-12 and IL-23, which could explain the effect on T cells. These properties of HP-NAP make it a potential immunotherapeutic tool to redirect harmful TH2 cell responses, as seen in atopic allergy, to TH1 cell responses and also in IL-12 induction in cancer therapy.
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