作者: Kathryn A. Eaton , Megan Mefford , Tracy Thevenot
DOI: 10.4049/JIMMUNOL.166.12.7456
关键词:
摘要: Gastritis due to Helicobacter pylori in mice and humans is considered a Th1-mediated disease, but the specific cell subsets cytokines involved are still not well understood. The goal of this study was investigate immunopathogenesis H. -induced gastritis delayed-type hypersensitivity (DTH) mice. C57BL/6- Prkdc scid were infected with reconstituted CD4 + , CD4-depleted, CD45RB high or low splenocytes from wild-type C57BL/6 IFN-γ −/− IL-10−/− Four eight weeks after transfer, DTH Ags determined by footpad injection; bacterial colonization quantified; secretion response Ag determined. present recipients unfractionated splenocytes, absent other groups. correlated gastritis, although all groups secreted some IFN-γ. most severe IL-10-deficient mice, least those given IFN-γ-deficient splenocytes. Bacterial inversely gastritis. These data indicate that 1) T cells both necessary sufficient for mice; 2) expression marker gastritis-inducing cells; 3) contributes IL-10 suppresses it, alone induce results support assertion mediated Th1-biased cellular immune response.