ArticleProceedings of the National Academy of Sciences of the United States of America2009
Transcriptional regulator Id2 controls survival of hepatic NKT cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
48 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Primordial Cells Bridging the Gap Between Innate and Adaptive Immunity.Advances in experimental medicine and biology · 2025Review
- ID2 promotes tumor progression and metastasis in thyroid cancer.Endocrine · 2024Article
- Insights into the heterogeneity of iNKT cells: tissue-resident and circulating subsets shaped by local microenvironmental cues.Frontiers in immunology · 2024Review
- Helix-Loop-Helix Proteins in Adaptive Immune Development.Frontiers in immunology · 2022Review
- Thymic development of unconventional T cells: how NKT cells, MAIT cells and γδ T cells emerge.Nature reviews. Immunology · 2020Review
- The Transcriptional Regulator Id2 Is Critical for Adipose-Resident Regulatory T Cell Differentiation, Survival, and Function.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Transcription factor YY1 is essential for iNKT cell development.Cellular & molecular immunology · 2019Article
- Lymphocyte innateness defined by transcriptional states reflects a balance between proliferation and effector functions.Nature communications · 2019Article
- The Roles of Liver-Resident Lymphocytes in Liver Diseases.Frontiers in immunology · 2019Review
- Tissue-specific functions of invariant natural killer T cells.Nature reviews. Immunology · 2018Review
- Development of mucosal-associated invariant T cells.Immunology and cell biology · 2018Review
- FOXO1 opposition of CD8Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Temporal regulation of Wnt/β-catenin signaling is important for invariant NKT cell development and terminal maturation.Molecular immunology · 2017Article
- Histone demethylases UTX and JMJD3 are required for NKT cell development in mice.Cell & bioscience · 2017Article
- All work and no Id2 makes a dull NKT cell.Immunology and cell biology · 2016Article
- Id2 regulates hyporesponsive invariant natural killer T cells.Immunology and cell biology · 2016Article
- Review
- The transcriptional programs of iNKT cells.Seminars in immunology · 2015Review
- Transcription factor networks directing the development, function, and evolution of innate lymphoid effectors.Annual review of immunology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Natural killer T cells expressing an invariant T-cell receptor (iNKT) regulate activation of both innate and adaptive immunity in many contexts. iNKT cells accumulate in the liver and rapidly produce prodigious amounts of numerous cytokines upon activation, impacting the immune response to viral infection, immunosurveillance for malignant cells, and liver regeneration. However, little is known about the factors controlling iNKT homeostasis, survival and hepatic localization. Here, we report that the absence of the transcriptional regulator Id2 resulted in a severe, intrinsic defect in the accumulation of hepatic iNKT cells. Id2-deficient iNKT cells showed increased cell death in the liver, although migration and functional activity were not impaired in comparison to Id2-expressing iNKT cells. Id2-deficient iNKT cells exhibited diminished expression of CXCR6, a critical determinant of iNKT cell accumulation in the liver, and of the anti-apoptotic molecules bcl-2 and bcl-X(L), compared to Id2-sufficient iNKT cells. Furthermore, survival and accumulation of iNKT cells lacking Id2 expression was rescued by deficiency in bim, a key pro-apoptotic molecule. Thus, Id2 was necessary to establish a hepatic iNKT cell population, defining a role for Id2 and implicating the Id targets, E protein transcription factors, in the regulation of iNKT cell homeostasis.
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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.