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Journal ArticleDOI

Activation of NK Cells and T Cells by NKG2D, a Receptor for Stress-Inducible MICA

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TLDR
An activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses is defined.
Abstract
Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.

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Innate and adaptive lymphoid cells in the human liver

TL;DR: The liver contains a heterogeneity of lymphoid cells with diverse recognition mechanisms and functions as mentioned in this paper, and these mediators of innate immunity against infectious pathogens and malignant cells respond immediately to stimuli and function as a temporal bridge for the adaptive immune response.
Journal ArticleDOI

Disulphide-isomerase-enabled shedding of tumour-associated NKG2D ligands

TL;DR: A molecular mechanism whereby domain-specific deconstruction regulates MICA protein shedding is uncovered, thereby promoting tumour immune evasion, and identifying surface ERp5 as a strategic target for therapeutic intervention is identified.
Journal ArticleDOI

CD28 extinction in human T cells: altered functions and the program of T‐cell senescence

TL;DR: Results of replicative senescence studies show thatCD28null T cells are derived from CD28+ precursors that have undergone repeated stimulation, indicating that CD28 silencing underlies the program of T‐cell aging.
Journal ArticleDOI

Natural Killer Cell Cytotoxicity Is Suppressed by Exposure to the Human NKG2D Ligand MICA*008 That Is Shed by Tumor Cells in Exosomes

TL;DR: In this paper, the authors reported shedding of the most frequently expressed MICA allele in human populations (MICA*008) into exosomes, small membrane vesicles that are secreted upon fusion with the plasma membrane.
References
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Journal ArticleDOI

Selective rejection of H–2-deficient lymphoma variants suggests alternative immune defence strategy

TL;DR: It is shown that murine lymphoma cells selected for loss of H–2 expression are less malignant after low-dose inoculation in syngeneic hosts than are wild-type cells, and that the rejection of such cells is non-adaptive.
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HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C

TL;DR: The identification of ligands for HLA-E is reported, which shows that a subset of HLA class I alleles has been shown to inhibit killing by CD94/NKG2A+ NK-cell clones, and only the HLA alleles that possess a leader peptide capable of upregulating Hla-E surface expression confer resistance toNK-cell-mediated lysis.
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Nk cell receptors

TL;DR: Three distinct receptor families, Ly49, CD94/NKG2, and KIR, are involved in NK cell recognition of polymorphic MHC class I molecules and a common pathway of inhibitory signaling is provided by ITIM sequences in the cytoplasmic domains of these otherwise structurally diverse receptors.
Journal ArticleDOI

Cloning the differences between two complex genomes.

TL;DR: The analysis of the differences between two complex genomes holds promise for the discovery of infectious agents and probes useful for genetic studies, and may also be used for isolating probes linked to sites of genomic rearrangements.
Journal ArticleDOI

Recognition of Stress-Induced MHC Molecules by Intestinal Epithelial γδ T Cells

TL;DR: In this paper, the expression and recognition of a major histocompatibility complex (MHC) class I-related molecule, MICA, matches this localization, and the closely related MICB were recognized by intestinal epithelial T cells expressing diverse Vδ1 γδ TCRs.
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