ReviewFrontiers in immunology2019
Implicating the Role of GILZ in Glucocorticoid Modulation of T-Cell Activation.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Induction treatment of lupus nephritis: to pulse or not to pulse? Whether 'tis nobler to universally or selectively prescribe.Lupus science & medicine · 2026Pooled it
- Review
- Inter-Organ Communication Networks in Systemic Physiology: Glucocorticoid Receptor α as a Central Integrator of Homeostasis.International journal of molecular sciences · 2026Review
- Potential Benefits of Metformin Via Roseburia Intestinalis in High-fat Diet-fed Mice With Colorectal Adenomas.Probiotics and antimicrobial proteins · 2026Article
- CAR-T manufacturing reduces heterogeneity between CIDP and multiple myeloma patient-derived T cells.Theranostics · 2026Article
- Glucocorticoid-induced leucine zipper as a context-dependent central integrator of innate and adaptive immune homeostasis.Frontiers in immunology · 2026Review
- Machine learning and transcriptomic analysis identify tubular injury biomarkers in patients with chronic kidney disease.International urology and nephrology · 2025Article
- Impact of glucocorticoid receptor polymorphism rs6198 on sepsis survival in a prospective multicenter cohort.Scientific reports · 2025Article
- The immunosuppressive effect of glucocorticoids in human primary T cells is mainly mediated via a rapid inhibition of the IL-2/IL-2R signaling axis.Cell communication and signaling : CCS · 2025Article
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- The dual role of glucocorticoids in the breast cancer immune microenvironment: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Co-Stimulation with TWEAK and TGF-β1 Induces Steroid-Insensitive TSLP and CCL5 Production in BEAS-2B Human Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- Intratumoral radiation dose heterogeneity augments antitumor immunity in mice and primes responses to checkpoint blockade.Science translational medicine · 2024Article
- Article
- Body mass, neuro-hormonal stress processing, and disease activity in lean to obese people with multiple sclerosis.Journal of neurology · 2024Article
- The Association between the rs3747406 Polymorphism in the Glucocorticoid-Induced Leucine Zipper Gene and Sepsis Survivals Depends on the SOFA Score.International journal of molecular sciences · 2024Article
- Pregnenolone sulfate induces transcriptional and immunoregulatory effects on T cells.Scientific reports · 2024Article
- Integrative analysis of neuroblastoma by single-cell RNA sequencing identifies the NECTIN2-TIGIT axis as a target for immunotherapy.Cancer cell · 2024Article
- Immunomodulation by glucocorticoid-induced leucine zipper in macrophages: enhanced phagocytosis, protection from pyroptosis, and altered mitochondrial function.Frontiers in immunology · 2024Article
- Evaluation of Genes and Molecular Pathways Involved in the Progression of Monoclonal Gammopathy of Undetermined Significance (MGUS) to Multiple Myeloma: A Systems Biology Approach.Molecular biotechnology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid-induced leucine zipper (GILZ) is a protein with multiple biological roles that is upregulated by glucocorticoids (GCs) in both immune and non-immune cells. Importantly, GCs are immunosuppressive primarily due to their regulation of cell signaling pathways that are crucial for immune system activity. GILZ, which is transcriptionally induced by the glucocorticoid receptor (GR), mediates part of these immunosuppressive, and anti-inflammatory effects, thereby controlling immune cell proliferation, survival, and differentiation. The primary immune cells targeted by the immunosuppressive activity of GCs are T cells. Importantly, the effects of GCs on T cells are partially mediated by GILZ. In fact, GILZ regulates T-cell activation, and differentiation by binding and inhibiting factors essential for T-cell function. For example, GILZ associates with nuclear factor-κB (NF-κB), c-Fos, and c-Jun and inhibits NF-κB-, and AP-1-dependent transcription. GILZ also binds Raf and Ras, inhibits activation of Ras/Raf downstream targets, including mitogen-activated protein kinase 1 (MAPK1). In addition GILZ inhibits forkhead box O3 (FoxO3) without physical interaction. GILZ also promotes the activity of regulatory T cells (Tregs) by activating transforming growth factor-β (TGF-β) signaling. Ultimately, these actions inhibit T-cell activation and modulate the differentiation of T helper (Th)-1, Th-2, Th-17 cells, thereby mediating the immunosuppressive effects of GCs on T cells. In this mini-review, we discuss how GILZ mediates GC activity on T cells, focusing mainly on the therapeutic potential of this protein as a more targeted anti-inflammatory/immunosuppressive GC therapy.
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