ArticleFrontiers in immunology2020
MICAgen Mice Recapitulate the Highly Restricted but Activation-Inducible Expression of the Paradigmatic Human NKG2D Ligand MICA.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- NKG2D ligand expression on NK cells induces NKG2D-mediated cross-tolerization of cytokine signaling and reduces NK cell tumor immunity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- CLN-619, a MICA/B monoclonal antibody that promotes innate immune cell-mediated antitumor activity.Journal for immunotherapy of cancer · 2025Article
- ULBP2 Promotes Tumor Progression by Suppressing NKG2D-Mediated Anti-Tumor Immunity.International journal of molecular sciences · 2025Article
- Targeting senescent cells with NKG2D-CAR T cells.Cell death discovery · 2024Article
- Nanobody-based CAR NK cells for possible immunotherapy of MICAPNAS nexus · 2024Article
- Oncolytic adenovirus coding for shedding-resistant MICA enhances immune responses against tumors.Cancer immunology, immunotherapy : CII · 2024Article
- Radiosensitization effect by HDAC inhibition improves NKG2D-dependent natural killer cytotoxicity in hepatocellular carcinoma.Frontiers in oncology · 2022Article
- Manipulating the NKG2D Receptor-Ligand Axis Using CRISPR: Novel Technologies for Improved Host Immunity.Frontiers in immunology · 2021Article
- Targeting MICA/B with cytotoxic therapeutic antibodies leads to tumor control.Open research Europe · 2021Article
- KIR+ CD8+ T Lymphocytes in Cancer Immunosurveillance and Patient Survival: Gene Expression Profiling.Cancers · 2020Article
- NKG2D and MICA/B shedding: a 'tag game' between NK cells and malignant cells.Clinical & translational immunology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NKG2D is a potent activating immunoreceptor expressed on nearly all cytotoxic lymphocytes promoting their cytotoxicity against self-cells expressing NKG2D ligands (NKG2DLs). NKG2DLs are MHC class I-like glycoproteins that usually are not expressed on "healthy" cells. Rather, their surface expression is induced by various forms of cellular stress, viral infection, or malignant transformation. Hence, cell surface NKG2DLs mark "dangerous" cells for elimination by cytotoxic lymphocytes and therefore can be considered as "kill-me" signals. In addition, NKG2DLs are up-regulated on activated leukocytes, which facilitates containment of immune responses. While the NKG2D receptor is conserved among mammals, NKG2DL genes have rapidly diversified during mammalian speciation, likely due to strong selective pressures exerted by species-specific pathogens. Consequently, NKG2DL genes are not conserved in man and mice, although their NKG2D-binding domains maintained structural homology. Human NKG2DLs comprise two members of the MIC (MICA/MICB) and six members of the ULBP family of glycoproteins (ULBP1-6) with MICA representing the best-studied human NKG2DLs by far. Many of these studies implicate a role of MICA in various malignant, infectious, or autoimmune diseases. However, conclusions from these studies often were limited in default of supporting
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