ArticleJournal of immunology (Baltimore, Md. : 1950)2011
TCR-dependent and -independent activation underlie liver-specific regulation of NKT cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Pyruvate kinase muscle 2 (PKM2) promotes CD4 T cell survival by regulating pyruvate oxidation during homeostasis and expansion.Science advances · 2026Article
- Understanding, predicting and achieving liver transplant tolerance: from bench to bedside.Nature reviews. Gastroenterology & hepatology · 2020Review
- JNK2 modulates the CD1d-dependent and -independent activation of iNKT cells.European journal of immunology · 2019Article
- The Role of Adaptor Proteins in the Biology of Natural Killer T (NKT) Cells.Frontiers in immunology · 2019Review
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- Multiple layers of transcriptional regulation by PLZF in NKT-cell development.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Serum-based tracking of de novo initiated liver cancer progression reveals early immunoregulation and response to therapy.Journal of hepatology · 2015Article
- NKT cells can help mediate the protective effects of 1,25-dihydroxyvitamin D3 in experimental autoimmune encephalomyelitis in mice.International immunology · 2015Article
- Natural killer T (NKT) cells in autoimmune hepatitis.Current opinion in immunology · 2013Review
- In-vivo stimulation of macaque natural killer T cells with α-galactosylceramide.Clinical and experimental immunology · 2013Article
- Exosome-like nanoparticles from intestinal mucosal cells carry prostaglandin E2 and suppress activation of liver NKT cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Intestinal mucus-derived nanoparticle-mediated activation of Wnt/β-catenin signaling plays a role in induction of liver natural killer T cell anergy in mice.Hepatology (Baltimore, Md.) · 2013Article
- Synthesis of amino core compounds of galactosyl phytosyl ceramide analogs for developing iNKT-cell inducers.Molecules (Basel, Switzerland) · 2012Article
- The split personality of NKT cells in malignancy, autoimmune and allergic disorders.Immunotherapy · 2011Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
The fate of invariant NKT (iNKT) cells following activation remains controversial and unclear. We systemically examined how iNKT cells are regulated following TCR-dependent and -independent activation with α-galactosylceramide (αGC) or IL-18 plus IL-12, respectively. Our studies reveal activation by αGC or IL-18 plus IL-12 induced transient depletion of iNKT cells exclusively in the liver that was independent of caspase 3-mediated apoptosis. The loss of iNKT cells was followed by repopulation and expansion of phenotypically distinct cells via different mechanisms. Liver iNKT cell expansion following αGC, but not IL-18 plus IL-12, treatment required an intact spleen and IFN-γ. Additionally, IL-18 plus IL-12 induced a more prolonged expansion of liver iNKT cells compared with αGC. iNKT cells that repopulate the liver following αGC had higher levels of suppressive receptors PD-1 and Lag3, whereas those that repopulate the liver following IL-18 plus IL-12 had increased levels of TCR and ICOS. In contrast to acute treatment that caused a transient loss of iNKT cells, chronic αGC or IL-18 plus IL-12 treatment caused long-term systemic loss requiring an intact thymus for repopulation of the liver. This report reveals a previously undefined role for the liver in the depletion of activated iNKT cells. Additionally, TCR-dependent and -independent activation differentially regulate iNKT cell distribution and phenotype. These results provide new insights for understanding how iNKT cells are systemically regulated following activation.
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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.