Binding ofEscherichia coliadhesin AfaE to CD55 triggers cell-surface expression of the MHC class I-related molecule MICA
NKG2D
DOI:
10.1073/pnas.032668099
Publication Date:
2002-07-26T14:37:36Z
AUTHORS (8)
ABSTRACT
MICA are distant homologs of MHC class I molecules expressed in the normal intestinal epithelium. They ligands NKG2D activating receptor on most γδ T cells, CD8+ αβ and natural killer cells therefore play a critical role innate immune responses. We investigated cell-surface expression infection epithelial cell lines by enteric bacteria show here that can be markedly increased diffusely adherent Escherichia coli diarrheagenic group. This effect is mediated specific interaction between bacterial adhesin AfaE its cellular receptor, CD55, or decay-accelerating factor. It extremely rapid after binding, consistent with stress-induced signal. induction triggered IFN-γ release expressing line NKL. host–bacteria pathway could pathogenesis inflammatory bowel disease, condition implicates trigger genetically susceptible individuals. was supported at surface colonic biopsies from Crohn's disease-affected patients compared controls.
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