ArticlePLoS pathogens2017
Voltage-dependent calcium channel signaling mediates GABAA receptor-induced migratory activation of dendritic cells infected by Toxoplasma gondii.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 59 citations in OpenAlex.
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Brain endothelial spheroids and cortical organoids reveal the impact of Toxoplasma gondii lineage and host-phagocyte-pathogen interactions on colonization.Cellular and molecular life sciences : CMLS · 2026Article
- Neurotransmitters as regulators of autoimmunity: mechanisms and translational targeting.NPJ autoimmunity · 2026Review
- ICAM-1/CD18-mediated sequestration of parasitized phagocytes in cortical capillaries promotes neuronal colonization by Toxoplasma gondii.Nature communications · 2025Article
- Cytoskeletal alterations in neuronal cells implicate Toxoplasma gondii secretory machinery and host microRNA-containing extracellular vesicles.Scientific reports · 2025Article
- Toxoplasma-induced behavior changes - is microbial dysbiosis the missing link?Frontiers in cellular and infection microbiology · 2024Review
- Overexpression of Eimeria tenella Rhoptry Kinase 2 Induces Early Production of Schizonts.Microbiology spectrum · 2023Article
- CaBritish journal of pharmacology · 2023Review
- scDual-Seq ofFrontiers in immunology · 2023Article
- The link between immunity and hypertension in the kidney and heart.Frontiers in cardiovascular medicine · 2023Review
- The Toxoplasma effector GRA28 promotes parasite dissemination by inducing dendritic cell-like migratory properties in infected macrophages.Cell host & microbe · 2022Article
- Epigenetic Manipulation of Psychiatric Behavioral Disorders Induced byFrontiers in cellular and infection microbiology · 2022Review
- Impact of Plant-Based Foods and Nutraceuticals onFrontiers in nutrition · 2022Review
- Blood-brain barrier-restricted translocation ofeLife · 2021Article
- GABAergic signaling by cells of the immune system: more the rule than the exception.Cellular and molecular life sciences : CMLS · 2021Review
- Integrin-dependent migratory switches regulate the translocation of Toxoplasma-infected dendritic cells across brain endothelial monolayers.Cellular and molecular life sciences : CMLS · 2021Article
- The deubiquitinase OTUB1 augments NF-κB-dependent immune responses in dendritic cells in infection and inflammation by stabilizing UBC13.Cellular & molecular immunology · 2021Article
- GABA transporter sustains IL-1β production in macrophages.Science advances · 2021Article
- Epidemiology, Pathophysiology, Diagnosis, and Management of Cerebral Toxoplasmosis.Clinical microbiology reviews · 2021Review
- A motogenic GABAergic system of mononuclear phagocytes facilitates dissemination of coccidian parasites.eLife · 2020Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The obligate intracellular parasite Toxoplasma gondii exploits cells of the immune system to disseminate. Upon T. gondii-infection, γ-aminobutyric acid (GABA)/GABAA receptor signaling triggers a hypermigratory phenotype in dendritic cells (DCs) by unknown signal transduction pathways. Here, we demonstrate that calcium (Ca2+) signaling in DCs is indispensable for T. gondii-induced DC hypermotility and transmigration in vitro. We report that activation of GABAA receptors by GABA induces transient Ca2+ entry in DCs. Murine bone marrow-derived DCs preferentially expressed the L-type voltage-dependent Ca2+ channel (VDCC) subtype Cav1.3. Silencing of Cav1.3 by short hairpin RNA or selective pharmacological antagonism of VDCCs abolished the Toxoplasma-induced hypermigratory phenotype. In a mouse model of toxoplasmosis, VDCC inhibition of adoptively transferred Toxoplasma-infected DCs delayed the appearance of cell-associated parasites in the blood circulation and reduced parasite dissemination to target organs. The present data establish that T. gondii-induced hypermigration of DCs requires signaling via VDCCs and that Ca2+ acts as a second messenger to GABAergic signaling via the VDCC Cav1.3. The findings define a novel motility-related signaling axis in DCs and unveil that interneurons and DCs share common GABAergic motogenic pathways. T. gondii employs GABAergic non-canonical pathways to induce host cell migration and facilitate dissemination.
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