Transcription profiling of intraepithelial and peripheral CTL from patients with celiac disease or cytomegalovirus seropositive patients suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases.

ABSTRACT: Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon g–producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor s

ORGANISM(S): Homo sapiens

DISEASE(S): cytomegalovirus seropositive

SUBMITTER: Bana Jabri 

PROVIDER: E-GEOD-4592 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress