ArticleJournal of immunology (Baltimore, Md. : 1950)2008
IP3 receptor-mediated Ca2+ release in naive CD4 T cells dictates their cytokine program.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Molecular insights into T cell development, activation and signal transduction (Review).Biomedical reports · 2025Review
- Type 3 IP3 receptor: Its structure, functions, and related disease implications.Channels (Austin, Tex.) · 2023Review
- Point mutations in the gene encoding IP3 receptor subtype 3 cause impairment in T-cell and B-cell immune responses via dysfunctional CaCellular & molecular immunology · 2023Article
- Immune dysregulation in depression: Evidence from genome-wide association.Brain, behavior, & immunity - health · 2020Article
- Protein Palmitoylation in Leukocyte Signaling and Function.Frontiers in cell and developmental biology · 2020Review
- Melatonin regulation of transcription in the reversal of morphine tolerance: Microarray analysis of differential gene expression.International journal of molecular medicine · 2019Article
- Modulation of intracellular calcium signaling by microRNA-34a-5p.Cell death & disease · 2018Article
- CalQuoScientific reports · 2017Article
- ITPR3 gene haplotype is associated with cervical squamous cell carcinoma risk in Taiwanese women.Oncotarget · 2017Article
- Phosphoproteomics Reveals Regulatory T Cell-Mediated DEF6 Dephosphorylation That Affects Cytokine Expression in Human Conventional T Cells.Frontiers in immunology · 2017Article
- Computational properties of mitochondria in T cell activation and fate.Open biology · 2016Review
- The Role of the Transcription Factor Ets1 in Lupus and Other Autoimmune Diseases.Critical reviews in immunology · 2016Article
- Article
- Shotgun proteomics: identification of unique protein profiles of apoptotic bodies from biliary epithelial cells.Hepatology (Baltimore, Md.) · 2014Article
- ETS1 variants confer susceptibility to ankylosing spondylitis in Han Chinese.Arthritis research & therapy · 2014Article
- Ets-1 facilitates nuclear entry of NFAT proteins and their recruitment to the IL-2 promoter.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Review of Ets1 structure, function, and roles in immunity.Cellular and molecular life sciences : CMLS · 2013Review
- Bidirectional coupling between ryanodine receptors and Ca2+ release-activated Ca2+ (CRAC) channel machinery sustains store-operated Ca2+ entry in human T lymphocytes.The Journal of biological chemistry · 2012Article
- Molecular mechanisms of treg-mediated T cell suppression.Frontiers in immunology · 2012Article
- NFATc1 affects mouse splenic B cell function by controlling the calcineurin--NFAT signaling network.The Journal of experimental medicine · 2011Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
IP(3) (inositol 1,4,5-trisphosphate) receptors (IP(3)Rs) regulate the release of Ca(2+) from intracellular stores in response to IP(3). Little is known about regulation of the expression of IP(3)Rs and their role during the activation of CD4 T cells. In this study we show that mouse naive CD4 T cells express IP(3)R1, IP(3)R2, and IP(3)R3, but that gene expression of IP(3)R3 primarily is down-regulated upon activation due to loss of the Ets-1 transcription factor. Down-regulation of IP(3)R expression in activated CD4 T cells is associated with the failure of TCR ligation to trigger Ca(2+) release in these cells. We also show that down-regulation of specific IP(3)Rs in activated CD4 T cells correlates with the requirement of IP(3)R-mediated Ca(2+) release only for the induction of, but not for the maintenance of, IL-2 and IFN-gamma expression. Interestingly, while inhibition of IP(3)R function early during activation blocks IL-2 and IFN-gamma production, it promotes the production of IL-17 by CD4 T cells. Thus, IP(3)Rs play a key role in the activation and differentiation of CD4 T cells. The immunosuppressive effect of pharmacological blockers of these receptors may be complicated by promoting the development of inflammatory CD4 T cells.
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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.