ArticleJournal of cellular and molecular medicine2015
Up-regulation of galectin-9 induces cell migration in human dendritic cells infected with dengue virus.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Search for Potential VDR/Partner Composite Elements in Regulatory DNA of Genes Associated with Respiratory Infections and Atopic Diseases.International journal of molecular sciences · 2025Article
- Galectin-9 regulates dendritic cell polarity and uropod contraction by modulating RhoA activity.The Journal of cell biology · 2025Article
- Unlocking Medical Breakthroughs: The Transformative Role of Case Reports in Clinical Discovery.Reports (MDPI) · 2025Article
- MGAT4A/Galectin9-Driven N-Glycosylation Aberration as a Promoting Mechanism for Poor Prognosis of Endometrial Cancer with TP53 Mutation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Expression of Gal-9 on Dendritic Cells and Soluble Forms of TIM-3/Gal-9 in Patients Suffering from Endometriosis.International journal of molecular sciences · 2023Article
- Secreted filarial nematode galectins modulate host immune cells.Frontiers in immunology · 2022Article
- CCL19 enhances CD8Journal of gastroenterology · 2021Article
- Blood Levels of Galectin-9, an Immuno-Regulating Molecule, Reflect the Severity for the Acute and Chronic Infectious Diseases.Biomolecules · 2021Review
- Detecting Allele-Specific Alternative Splicing from Population-Scale RNA-Seq Data.American journal of human genetics · 2020Article
- Study of T-cell immunoglobulin and mucin domain-3 expression profile in peripheral blood and bone marrow of human acute lymphoblastic leukemia patients.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020Article
- Immunomodulatory Dual-Sized Microparticle System Conditions Human Antigen Presenting Cells Into a Tolerogenic PhenotypeFrontiers in immunology · 2020Article
- Intracellular Galectin-9 Controls Dendritic Cell Function by Maintaining Plasma Membrane Rigidity.iScience · 2019Article
- CCL19 and CCR7 Expression, Signaling Pathways, and Adjuvant Functions in Viral Infection and Prevention.Frontiers in cell and developmental biology · 2019Review
- Signaling of Macrophage Inflammatory Protein (MIP)-3β Facilitates Dengue Virus-Induced Microglial Cell Migration.Viruses · 2018Article
- Acute stimulation generates Tim-3-expressing T helper type 1 CD4 T cells that persist in vivo and show enhanced effector function.Immunology · 2018Article
- Bioinformatics analysis of fibroblasts exposed to TGF‑β at the early proliferation phase of wound repair.Molecular medicine reports · 2017Article
- Translational Implication of Galectin-9 in the Pathogenesis and Treatment of Viral Infection.International journal of molecular sciences · 2017Review
- Secretion of Galectin-9 as a DAMP during Dengue Virus Infection in THP-1 Cells.International journal of molecular sciences · 2017Article
- Dengue virus infection increases microglial cell migration.Scientific reports · 2017Article
- Regulation of Eosinophil Recruitment and Activation by Galectins in Allergic Asthma.Frontiers in medicine · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-9 (Gal-9) exerts immunosuppressive effects by inducing apoptosis in T cells that produce interferon-γ and interleukin (IL)-17. However, Gal-9 can be pro-inflammatory in lipopolysaccharide-stimulated monocytes. Using microarray analysis, we observed that Gal-9 was up-regulated in human dendritic cells (DCs) after dengue virus (DV) infection. The investigation into the immunomodulatory effects and mechanisms of Gal-9 in DCs exposed to DV revealed that DV infection specifically increased mRNA and protein levels of Gal-9 but not those of Gal-1 or Gal-3. Blocking p38, but not c-Jun N-terminal kinase or extracellular signal-regulated kinase (ERK), inhibited DV-induced expression of Gal-9. Reduction in Gal-9 by small interference RNA treatment suppressed DV-stimulated migration of DCs towards the chemoattractants CCL19 and CCL21. In addition, DV-induced IL-12p40 production was reduced after knockdown of Gal-9 in DCs. Furthermore, Gal-9 deficiency suppressed DV-induced activation of nuclear factor-κB. Inhibition of DV-induced DC migration under conditions of Gal-9 deficiency was mediated through suppressing ERK activation but not by regulating the expression of CCR7, the receptor for CCL19 and CCL21. Both the reduction in IL-12 production and the suppression of ERK activity might account for the inhibition of DV-induced DC migration after knockdown of Gal-9. In summary, this study reveals the roles of Gal-9 in DV-induced migration of DCs. The findings indicate that Gal-9 might be a therapeutic target for preventing immunopathogenesis induced by DV infection.
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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.