Helicobacter pylori infection in immunized mice lacking major histocompatibility complex class I and class II functions

The role of major histocompatibility complex (MHC) class I- and class II-restricted functions in Helicobacter pylori infection and immunity upon oral immunization was examined in vivo. Experimental challenge with H. pylori SS1 resulted in significantly greater (P less than or equal to 0.025) colonization of MHC class I and class II mutant mice than C57BL/6 wild-type mice. Oral immunization with H. pylori whole-cell lysates and cholera toxin adjuvant significantly reduced the magnitude of H. pylori infection in C57BL/6 wild-type (P = 0.0083) and MHC class I knockout mice (P = 0.0048), but it had no effect on the H. pylori infection level in MHC class II-deficient mice. Analysis of the anti-H. pylori antibody levels in serum showed a dominant serum immunoglobulin G1 (IgG1) response in immunized C57BL/6 wild-type and MHC class I mutant mice but no detectable serum IgG response in MHC class II knockout mice. Populations of T-cell-receptor (TCR) alpha beta(+) CD4(+) CD54(+) cells localized to gastric tissue of immunized C57BL/6 wild-type and MHC class I knockout mice, but TCR alpha beta(+) CD8(+) cells predominated in the gastric tissue of immunized MHC class II-deficient mice. These observations show that CD4(+) T cells engaged after mucosal immunization may be important for the generation of a protective anti-H. pylori immune response and that CD4(+) CD8(-) and CD4(-) CD8(+) T cells regulate the extent of H. pylori infection in vivo.