ArticleCell reports2014
GILZ promotes production of peripherally induced Treg cells and mediates the crosstalk between glucocorticoids and TGF-β signaling.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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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
77 citing papers in PubMed, 129 citations in OpenAlex.
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- Neuro-immune crosstalk in the tumor microenvironment: mechanisms and therapeutic implications for cancer immunotherapy.Journal of neuroinflammation · 2026Review
- Glucocorticoid-induced Leucine Zipper (GILZ) is a novel secreted protein by intestinal L-cells and is dysregulated during active ulcerative colitis.Cell death discovery · 2026Article
- Stress Biology in Cancer: Neuroendocrine-Immune Mechanisms Linking Tumor Progression to Translational Interventions.Cancer communications (London, England) · 2026Review
- Glucocorticoid-induced leucine zipper as a context-dependent central integrator of innate and adaptive immune homeostasis.Frontiers in immunology · 2026Review
- Immunomodulatory mechanisms of the gut microbiota and metabolites on regulatory T cells in rheumatoid arthritis.Frontiers in immunology · 2025Review
- Impact of corticosteroids on the efficacy of first-line pembrolizumab plus chemotherapy in patients with advanced non-small-cell lung cancer.Therapeutic advances in medical oncology · 2025Article
- CRISPR-GEM: A Novel Machine Learning Model for CRISPR Genetic Target Discovery and Evaluation.ACS synthetic biology · 2024Article
- High expression of L-GILZ transcript variant 1 (GILZ TV 1) is associated with increased 30-day sepsis mortality, and a high expression ratio possibly contraindicates hydrocortisone administration.Critical care (London, England) · 2024Article
- CRISPR-GEM: A Novel Machine Learning Model for CRISPR Genetic Target Discovery and Evaluation.bioRxiv : the preprint server for biology · 2024Article
- Augmenting regulatory T cells: new therapeutic strategy for rheumatoid arthritis.Frontiers in immunology · 2024Review
- Exploring the complex interplay: gut microbiome, stress, and leptospirosis.Frontiers in microbiology · 2024Review
- Role of histamine HInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Comprehensive bioinformatic analysis of the expression and prognostic significance of TSC22D domain family genes in adult acute myeloid leukemia.BMC medical genomics · 2023Article
- Immunosuppression for immune-related adverse events during checkpoint inhibition: an intricate balance.NPJ precision oncology · 2023Review
- Immunogenicity of Recombinant Adeno-Associated Virus (AAV) Vectors for Gene Transfer.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Review
- Learning from the nexus of autoimmunity and cancer.Immunity · 2023Review
- Chronic stress in solid tumor development: from mechanisms to interventions.Journal of biomedical science · 2023Review
- Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease.International journal of molecular sciences · 2023Article
- Differential distribution of steroid hormone signaling networks in the human choroid-retinal pigment epithelial complex.BMC ophthalmology · 2022Article
17 more citing papers are in PubMed but not listed here.
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10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulatory T (Treg) cells expressing the transcription factor forkhead box P3 (FoxP3) control immune responses and prevent autoimmunity. Treatment with glucocorticoids (GCs) has been shown to increase Treg cell frequency, but the mechanisms of their action on Treg cell induction are largely unknown. Here, we report that glucocorticoid-induced leucine zipper (GILZ), a protein induced by GCs, promotes Treg cell production. In mice, GILZ overexpression causes an increase in Treg cell number, whereas GILZ deficiency results in impaired generation of peripheral Treg cells (pTreg), associated with increased spontaneous and experimental intestinal inflammation. Mechanistically, we found that GILZ is required for GCs to cooperate with TGF-β in FoxP3 induction, while it enhances TGF-β signaling by binding to and promoting Smad2 phosphorylation and activation of FoxP3 expression. Thus, our results establish an essential GILZ-mediated link between the anti-inflammatory action of GCs and the regulation of TGF-β-dependent pTreg production.
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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.