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Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA.
TLDR
An activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses is defined. Expand
Tumour-derived soluble MIC ligands impair expression of NKG2D and T-cell activation
TLDR
It is shown that binding of MIC induces endocytosis and degradation of NKG2D, a mode of T-cell silencing that may promote tumour immune evasion and, by inference, compromise host resistance to infections. Expand
Cell stress-regulated human major histocompatibility complex class I gene expressed in gastrointestinal epithelium.
TLDR
A highly divergent human MHC class I molecule, MICA, encodes a cell surface glycoprotein, which is not associated with beta 2-microglobulin, is conformationally stable independent of conventional class I peptide ligands, and almost exclusively expressed in gastrointestinal epithelium. Expand
Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease.
TLDR
It is shown that, under conditions of dysregulated IL15 expression in vivo in patients with celiac disease and in vitro in healthy individuals, multiple steps of the NKG2D/DAP10 signaling pathway leading to ERK and JNK activation are coordinately primed to activate direct cytolytic function independent of TCR specificity in effector CD8 T cells. Expand
Interactions of human NKG2D with its ligands MICA, MICB, and homologs of the mouse RAE-1 protein family
TLDR
Comparison of allelic variants of MICA revealed large differences in NKG2D binding that were associated with a single amino acid substitution at position 129 in the α2 domain, which indicated promiscuous modes of receptor binding. Expand
Recognition of stress-induced MHC molecules by intestinal epithelial gammadelta T cells.
TLDR
With intestinal epithelial cell lines, the expression and recognition of MICA and MICB could be stress-induced and these molecules may broadly regulate protective responses by the Vdelta1 gammadelta T cells in the epithelium of the intestinal tract. Expand
Stimulation of T cell autoreactivity by anomalous expression of NKG2D and its MIC ligands in rheumatoid arthritis
TLDR
The results suggest that a profound dysregulation of NKG2D and its MIC ligands may cause autoreactive T cell stimulation, thus promoting the self-perpetuating pathology in RA and possibly other autoimmune diseases. Expand
Promoter Region Architecture and Transcriptional Regulation of the Genes for the MHC Class I-Related Chain A and B Ligands of NKG2D1
TLDR
Results reveal distinct modes of activation of the genes for the MIC ligands of NKG2D and provide a molecular framework for analyses of gene regulation under different cellular insult conditions. Expand
Broad tumor-associated expression and recognition by tumor-derived gamma delta T cells of MICA and MICB.
TLDR
MICA/B are tumor-associated antigens that can be recognized, in an apparently unconditional manner, by a subset of tumor-infiltrating gamma delta T cells, and raise the possibility that an induced expression of MICA/ B, by conditions that may be related to tumor homeostasis and growth, could play a role in immune responses against tumors. Expand
Costimulation of CD8alphabeta T cells by NKG2D via engagement by MIC induced on virus-infected cells.
TLDR
It is found that infection by cytomegalovirus resulted in substantial increases in MIC on cultured fibroblast and endothelial cells and was associated with induced MIC expression in interstitial pneumonia and NKG2D functioned as a costimulatory receptor that can substitute for CD28. Expand
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