ArticleEMBO reports2020
ER stress in antigen-presenting cells promotes NKT cell activation through endogenous neutral lipids.
Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- The α glycolipid rules the NKT cell TCR.The Journal of experimental medicine · 2025Article
- Lipidomic scanning of self-lipids identifies headless antigens for natural killer T cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Endoplasmic Reticulum Stress in Hypertension and Salt Sensitivity of Blood Pressure.Current hypertension reports · 2024Review
- The surveillance of viral infections by the unconventional Type I NKT cell.Frontiers in immunology · 2024Review
- Host Lipid Manipulation by Intracellular Bacteria: Moonlighting for Immune Evasion.The Journal of membrane biology · 2023Review
- Article
- CD1-mediated immune responses in mucosal tissues: molecular mechanisms underlying lipid antigen presentation system.Experimental & molecular medicine · 2023Review
- Activation of cDCs and iNKT cells contributes to triptolide-induced hepatotoxicity via STING signaling pathway and endoplasmic reticulum stress.Cell biology and toxicology · 2023Article
- A bispecific T cell engager recruits both type 1 NKT and Vγ9Vδ2-T cells for the treatment of CD1d-expressing hematological malignancies.Cell reports. Medicine · 2023Article
- Review
- Selenoprotein K Is Essential for the Migration and Phagocytosis of Immature Dendritic Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Adoptive Immunotherapy With Engineered iNKT Cells to Target Cancer Cells and the Suppressive Microenvironment.Frontiers in medicine · 2022Review
- Multi-Omics Characterizes the Effects and Mechanisms of CD1d in Nonalcoholic Fatty Liver Disease Development.Frontiers in cell and developmental biology · 2022Article
- CD8Frontiers in immunology · 2022Review
- Harnessing invariant natural killer T cells to control pathological inflammation.Frontiers in immunology · 2022Review
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- Human intestinal and circulating invariant natural killer T cells are cytotoxic against colorectal cancer cells via the perforin-granzyme pathway.Molecular oncology · 2021Article
- Review
- Endoplasmic Reticulum Quality Control in Immune Cells.Frontiers in cell and developmental biology · 2021Review
- NKT Cells Contribute to the Control of Microbial Infections.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
CD1d-restricted invariant natural killer T (iNKT) cells constitute a common glycolipid-reactive innate-like T-cell subset with a broad impact on innate and adaptive immunity. While several microbial glycolipids are known to activate iNKT cells, the cellular mechanisms leading to endogenous CD1d-dependent glycolipid responses remain largely unclear. Here, we show that endoplasmic reticulum (ER) stress in APCs is a potent inducer of CD1d-dependent iNKT cell autoreactivity. This pathway relies on the presence of two transducers of the unfolded protein response: inositol-requiring enzyme-1a (IRE1α) and protein kinase R-like ER kinase (PERK). Surprisingly, the neutral but not the polar lipids generated within APCs undergoing ER stress are capable of activating iNKT cells. These data reveal that ER stress is an important mechanism to elicit endogenous CD1d-restricted iNKT cell responses through induction of distinct classes of neutral lipids.
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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.