Results 51 to 60 of about 381,426 (191)

Manipulating the NKG2D Receptor-Ligand Axis Using CRISPR: Novel Technologies for Improved Host Immunity

open access: yesFrontiers in Immunology, 2021
The activating immune receptor natural killer group member D (NKG2D) and its cognate ligands represent a fundamental surveillance system of cellular distress, damage or transformation.
Eric Alves   +11 more
doaj   +1 more source

Contrasting Effects of the Cytotoxic Anticancer Drug Gemcitabine and the EGFR Tyrosine Kinase Inhibitor Gefitinib on NK Cell-Mediated Cytotoxicity via Regulation of NKG2D Ligand in Non-Small-Cell Lung Cancer Cells. [PDF]

open access: yesPLoS ONE, 2015
Several cytotoxic anticancer drugs inhibit DNA replication and/or mitosis, while EGFR tyrosine kinase inhibitors inactivate EGFR signalling in cancer cell.
Riki Okita   +13 more
doaj   +1 more source

Anti-NKG2D single domain-based antibodies for the modulation of anti-tumor immune response

open access: yesOncoImmunology, 2021
The natural killer group 2 member D (NKG2D) receptor is a C-type lectin-like activating receptor mainly expressed by cytotoxic immune cells including NK, CD8+ T, γδ T and NKT cells and in some pathological conditions by a subset of CD4+ T cells. It binds
Adeline Raynaud   +7 more
doaj   +1 more source

Making Sense of the Diverse Ligand Recognition by NKG2D [PDF]

open access: yesThe Journal of Immunology, 2002
Abstract NKG2D recognizes multiple diverse ligands. Despite recent efforts in determining the crystal structures of NKG2D-ligand complexes, the principle governing this receptor-ligand recognition and hence the criteria for identifying unknown ligands of NKG2D remain central issues to be resolved.
Sergei, Radaev   +4 more
openaire   +2 more sources

Advanced Materials for Biologics Delivery to Brain Tumors

open access: yesAdvanced Materials, EarlyView.
Material innovation is central to unlocking the therapeutic potential of biologics against many central nervous system diseases, including brain cancer. By engineering carriers with controlled transport, targeting, and release properties, advanced materials can overcome the blood–brain barrier and tumor microenvironment, improving the delivery of ...
Yuran Feng   +4 more
wiley   +1 more source

NKG2D ligand expression in Crohn's disease and NKG2D-dependent stimulation of CD8+ T cell migration [PDF]

open access: yes, 2017
Interaction between the activating NKG2D receptor on lymphocytes and its ligands MICA, MICB, and ULBP1–6 modulate T and NK cell activity and may contribute to the pathogenesis of Crohn's disease (CD). NKG2D ligands are generally not expressed on the cell
Teis Jensen   +27 more
core   +1 more source

Receptor subtype-dependent effects of propofol on metalloproteinase activity, NKG2D ligand expression, and NK cell-mediated cytotoxicity in breast cancer: an in vitro study [PDF]

open access: yesKorean Journal of Anesthesiology
Background The effects of propofol, a commonly used intravenous anesthetic, on the breast cancer tumor microenvironment are not well understood. This study examined the influence of propofol on natural killer (NK) group 2, member D (NKG2D) ligand ...
Hyun-Su Ri   +7 more
doaj   +1 more source

Autonomous stimulation of cancer cell plasticity by the human NKG2D lymphocyte receptor coexpressed with its ligands on cancer cells. [PDF]

open access: yesPLoS ONE, 2014
The stimulatory NKG2D receptor on lymphocytes promotes tumor immune surveillance by targeting ligands selectively induced on cancer cells. Progressing tumors counteract by employing tactics to disable lymphocyte NKG2D.
Xin Cai   +8 more
doaj   +1 more source

Radiosensitization effect by HDAC inhibition improves NKG2D-dependent natural killer cytotoxicity in hepatocellular carcinoma

open access: yesFrontiers in Oncology, 2022
BackgroundHepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. Radiotherapy (RT) controls HCC unsatisfactorily and temporarily.
Yu-Fan Liu   +10 more
doaj   +1 more source

TP53 Loss Elevates NF‐κB‐IFN‐β‐MHC‐Ia Signaling to Promote NK Cell Resistance in Osteosarcoma

open access: yesAdvanced Science, EarlyView.
TP53 loss in a transforming or osteosarcoma cell promotes cytosolic DNA accumulation, activating NF‐κB‐dependent IFN‐β production. Autocrine IFN‐β signaling increases cell‐surface HLA‐Ia expression, strengthens inhibitory KIR signaling in natural killer cells, and thereby enables the affected cell to evade NK cell‐mediated cytotoxicity.
Guihui Qin   +9 more
wiley   +1 more source

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