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* Department of Clinical Immunology, University of Göteborg, Göteborg, Sweden;
Department of Immunology, AstraZeneca R&D Boston, Waltham, MA 02451; and
Department of Pathology, Örebro University Hospital, Örebro, Sweden
The regulatory roles of Th1 and Th2 cells in immune protection
against Helicobacter infection are not clearly
understood. In this study, we report that a primary H.
pylori infection can be established in the absence of IL-12 or
IFN-
. However, IFN-, but not IL-12, was involved in the
development of gastritis because IFN--/- (GKO) mice
exhibited significantly less inflammation as compared with
IL-12-/- or wild-type (WT) mice. Both
IL-12-/- and GKO mice failed to develop protection
following oral immunization with H. pylori lysate and
cholera toxin adjuvant. By contrast, Th2-deficient,
IL-4-/-, and WT mice were equally well protected. Mucosal
immunization in the presence of coadministered rIL-12 in WT mice
increased Ag-specific IFN--producing T cells by 5-fold and gave an
additional 4-fold reduction in colonizing bacteria, confirming a key
role of Th1 cells in protection. Importantly, only protected
IL-4-/- and WT mice demonstrated substantial influx of
CD4+ T cells in the gastric mucosa. The extent of
inflammation in challenged IL-12-/- and GKO mice was much
reduced compared with that in WT mice, indicating that IFN-/Th1
cells also play a major role in postimmunization gastritis. Of note,
postimmunization gastritis in IL-4-/- mice was
significantly milder than WT mice, despite a similar level of
protection, indicating that immune protection is not directly linked to
the degree of gastric inflammation. Only protected mice had T cells
that produced high levels of IFN- to recall Ag, whereas both
protected and unprotected mice produced high levels of IL-13. We
conclude that IL-12 and Th1 responses are crucial for H.
pylori-specific protective immunity.
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