1. Vaccinating Against Helicobacter pylori: Dissecting the Mechanism
Philip Sutton 
Gastroenterology 
Volume 141, Issue 4, Pages (October 2011)
DOI: /j.gastro
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2. Figure 1
Hypothetical model of PAR2 interactions in vaccine-induced protective immunity against H pylori. (1) H pylori infection recruits innate immune cells, including mast cells, neutrophils, and DCs to the gastric lamina propria. (2) PAR2-activating serine proteases are potentially produced by many sources, including mast cells, neutrophils, and bacteria. One or more of these serine proteases activate PAR2 expressed on DCs. (3) H pylori–specific T-helper cells (Th), induced by prior vaccination, are recruited to the site of infection. Activated DCs present H pylori antigen, as well as release IL-23 that induces a Th17-type immune response. This may potentially occur in the lymph nodes that drain the gastric mucosa or in the lamina propria itself. (4) Activated Th17 cells secrete IL-17 into the gastric mucosa. (5) IL-17 enhances the recruitment of neutrophils to the site of inflammation, likely resulting in the continued production of PAR2 activating serine protease. (6) IL-17, or another product of Th17 cells, induces an effector mechanism that nonspecifically reduces H pylori colonization. This effector mechanism is currently unknown, and may be of either immune or epithelial cell origin.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2011 AGA Institute Terms and Conditions