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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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Citations
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Journal ArticleDOI

Soluble NKG2D ligands: prevalence, release, and functional impact.

TL;DR: The available data on the prevalence, release, functional impact, and potential clinical value of sNKG2DL are reviewed and discussed.
Journal ArticleDOI

Signaling pathways engaged by NK cell receptors: double concerto for activating receptors, inhibitory receptors and NK cells.

TL;DR: Despite the absence of antigen-specific receptors at their surface, NK cells can selectively eliminate virus-infected cells, tumor cells and allogenic cells with remarkable structural and functional homologies with T cell- and B cell-antigen receptors.
Journal ArticleDOI

Immune functions of the skin.

TL;DR: The skin, the body's largest organ, helps to secure the integrity of the host and, at the same time, allows the individual to communicate with the outside world by providing a finely tuned balance between protection from harmful pathogens and bidirectional signal exchange.
Journal ArticleDOI

Cancers Related to Immunodeficiencies: Update and Perspectives

TL;DR: The importance of PID defects in the development of malignancies and the current limitations associated with molecular pathogenesis of these diseases are discussed and the need for further knowledge of how specific mutations can modulate the immune system to alter immunosurveillance is emphasized.
Journal ArticleDOI

IL-21 Down-Regulates NKG2D/DAP10 Expression on Human NK and CD8+ T Cells

TL;DR: Data indicate that IL-21 is able to channel NK and CD8+ T cell function by altering the expression pattern of activation/costimulatory receptors.
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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