ArticleBlood2015
Lack of glucocorticoid-induced leucine zipper (GILZ) deregulates B-cell survival and results in B-cell lymphocytosis in mice.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Kaposi sarcoma-associated herpesvirus cooperates with Epstein-Barr virus to co-transform a small set of human B cells oncogenically.PLoS pathogens · 2025Article
- Impact of immunosuppressive drugs on efficacy of mesenchymal stem cell therapy for suppressing renal fibrosis.Stem cells translational medicine · 2024Article
- Immunomodulation by glucocorticoid-induced leucine zipper in macrophages: enhanced phagocytosis, protection from pyroptosis, and altered mitochondrial function.Frontiers in immunology · 2024Article
- Dynamic RBM47 ISGylation confers broad immunoprotection against lung injury and tumorigenesis via TSC22D3 downregulation.Cell death discovery · 2023Article
- Role of histamine HInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Aprepitant plus palonosetron versus dexamethasone plus palonosetron in preventing chemotherapy-induced nausea and vomiting in patients with moderate-emetogenic chemotherapy: A randomized, open-label, phase 3 trial.EClinicalMedicine · 2022Article
- Review
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- Glucocorticoid-induced leucine zipper regulates liver fibrosis by suppressing CCL2-mediated leukocyte recruitment.Cell death & disease · 2021Article
- Deficit of glucocorticoid-induced leucine zipper amplifies angiotensin-induced cardiomyocyte hypertrophy and diastolic dysfunction.Journal of cellular and molecular medicine · 2021Article
- Murine Glucocorticoid Receptors Orchestrate B Cell Migration Selectively between Bone Marrow and Blood.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Regulation of the germinal center response by nuclear receptors and implications for autoimmune diseases.The FEBS journal · 2020Review
- Glucocorticoid-Induced Leucine Zipper: A Promising Marker for Monitoring and Treating Sepsis.Frontiers in immunology · 2020Review
- HSD11B1 is upregulated synergistically by IFNγ and TNFα and mediates TSG-6 expression in human UC-MSCs.Cell death discovery · 2020Article
- Ibrutinib reprograms the glucocorticoid receptor in chronic lymphocytic leukemia cells.Leukemia · 2019Article
- Relapse-associated AURKB blunts the glucocorticoid sensitivity of B cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Glucocorticoids and Glucocorticoid-Induced-Leucine-Zipper (GILZ) in Psoriasis.Frontiers in immunology · 2019Review
- Could GILZ Be the Answer to Glucocorticoid Toxicity in Lupus?Frontiers in immunology · 2019Review
- Glucocorticoid-Induced Leucine Zipper: A Novel Anti-inflammatory Molecule.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GC) are widely used as antiinflammatory/immunosuppressive drugs and antitumor agents in several types of lymphoma and leukemia. Therapeutic doses of GC induce growth-suppressive and cytotoxic effects on various leukocytes including B cells. Molecular mechanisms of GC action include induction of GC target genes. Glucocorticoid-induced leucine zipper (GILZ) is a rapidly, potently, and invariably GC-induced gene. It mediates a number of GC effects, such as control of cell proliferation, differentiation, and apoptosis. Here we show that deletion of GILZ in mice leads to an accumulation of B lymphocytes in the bone marrow, blood, and lymphoid tissues. Gilz knockout (KO) mice develop a progressive nonlethal B lymphocytosis, with expansion of B220(+) cells in the bone marrow and in the periphery, dependent on increased B-cell survival. Decreased B-cell apoptosis in mice lacking GILZ correlates with increased NF-κB transcriptional activity and Bcl-2 expression. B cell-specific gilz KO mice confirmed that the effect of GILZ deletion is B-cell self-intrinsic. These results establish GILZ as an important regulator of B-cell survival and suggest that the deregulation of GILZ expression could be implicated in the pathogenesis of B-cell disorders.
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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.