부산대학교 도서관

ABSTRACTThe role of major histocompatibility complex (MHC) class I- and class II-restricted functions in Helicobacter pyloriinfection and immunity upon oral immunization was examined in vivo. Experimental challenge with H. pyloriSS1 resulted in significantly greater (P≤ 0.025) colonization of MHC class I and class II mutant mice than C57BL/6 wild-type mice. Oral immunization with H. pyloriwhole-cell lysates and cholera toxin adjuvant significantly reduced the magnitude of H. pyloriinfection 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. pyloriinfection level in MHC class II-deficient mice. Analysis of the anti-H. pyloriantibody 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) αβ+CD4+CD54+cells localized to gastric tissue of immunized C57BL/6 wild-type and MHC class I knockout mice, but TCRαβ+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. pyloriimmune response and that CD4+CD8−and CD4−CD8+T cells regulate the extent of H. pyloriinfection in vivo.