ArticleJournal of innate immunity2014
Endothelial cell activation and proliferation modulate NKG2D activity by regulating MICA expression and shedding.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- NK cell dysregulation may potentiate cardiovascular disease in adolescents with perinatally acquired HIV on antiretroviral therapy.Nature communications · 2026Article
- Mechanisms of allorecognition and xenorecognition in transplantation.Clinical transplantation and research · 2024Review
- Bystander activated CD8Nature communications · 2024Article
- Bystander CD8 + T cells may be involved in the acute phase of diffuse alveolar damage.Virchows Archiv : an international journal of pathology · 2023Article
- Secretome and Tunneling Nanotubes: A Multilevel Network for Long Range Intercellular Communication between Endothelial Cells and Distant Cells.International journal of molecular sciences · 2021Review
- Induction of T Cell Senescence by Cytokine Induced Bystander Activation.Frontiers in aging · 2021Review
- Targeting MHC Regulation Using Polycyclic Polyprenylated Acylphloroglucinols Isolated fromBiomolecules · 2020Article
- Chimeric antigen receptor T-cell therapy for acute myeloid leukemia: how close to reality?Haematologica · 2019Article
- MICA and NKG2D: Is There an Impact on Kidney Transplant Outcome?Frontiers in immunology · 2017Review
- Immunomodulation of endothelial differentiated mesenchymal stromal cells: impact on T and NK cells.Immunology and cell biology · 2016Article
- Prenylated Polyphenols from Clusiaceae and Calophyllaceae with Immunomodulatory Activity on Endothelial Cells.PloS one · 2016Article
- MHC I-related chain a expression in gastric carcinoma and the efficacy of immunotherapy with cytokine-induced killer cells.American journal of cancer research · 2015Article
- The DNA Damage Response: A Common Pathway in the Regulation of NKG2D and DNAM-1 Ligand Expression in Normal, Infected, and Cancer Cells.Frontiers in immunology · 2014Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MICA are major histocompatibility complex class I-related molecules, expressed by endothelial cells (ECs), that may be targets for alloantibodies and NKG2D-expressing natural killer (NK) and T effector cells in organ allografts. This study shows that basal levels of MICA expressed on vascular ECs is sufficient to functionally modulate the expression and activity of the immunoreceptor NKG2D in allogeneic NK cells. We found that MICA expression is differentially regulated at the EC surface in response to cytokines. TNFα upregulates MICA while IFNγ significantly decreases MICA at the EC surface. Both cytokines induce the release of soluble MICA by ECs. Modulation of NKG2D correlates with the MICA level on the EC surface. Glycosylation and metalloproteinase activities account for major post-transcriptional mechanisms controlling MICA level and the function in ECs. Our results indicate that, in addition to the NFκB pathway, the mitogen-activated protein kinase pathways JNK, ERK1/2 and p38 are key signaling pathways in the control of MICA by the cytokines. Finally, we show that EC proliferation mediated by FGF-2 or wound healing increases the MICA level. Together, our data suggest that inflammation and proliferation regulate endothelial MICA expression and shedding, enabling ECs to modulate NKG2D activity on effector NK and T cells, and provide further evidence of a role for ECs in immunoregulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.