ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2010
Predominant interferon-γ-mediated expression of CXCL9, CXCL10, and CCL5 proteins in the brain during chronic infection with Toxoplasma gondii in BALB/c mice resistant to development of toxoplasmic encephalitis.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Gene expression profiling in cardiac tissue of mice chronically infected with Toxoplasma gondii: implications for immune response pathways.European journal of medical research · 2025Article
- The Absence of CXCL10 Activity Does Not Affect the Capability of CD8Microorganisms · 2024Article
- Article
- Glia Maturation Factor Beta: A Novel Neuro-Impairment Prediction Factor in Toxoplasmosis.Iranian journal of public health · 2024Article
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Transcriptome analysis of a newly established mouse model of Toxoplasma gondii pneumonia.Parasites & vectors · 2023Article
- IFN-γ production by brain-resident cells activates cerebral mRNA expression of a wide spectrum of molecules critical for both innate and T cell-mediated protective immunity to control reactivation of chronic infection withFrontiers in cellular and infection microbiology · 2023Article
- Behavioral Changes Induced by Latent Toxoplasmosis Could Arise from CNS Inflammation and Neuropathogenesis.Current topics in behavioral neurosciences · 2023Article
- Epidemiology, Pathophysiology, Diagnosis, and Management of Cerebral Toxoplasmosis.Clinical microbiology reviews · 2021Review
- P18 (SRS35/TgSAG4) Plays a Role in the Invasion and Virulence ofFrontiers in immunology · 2021Article
- Imiquimod Targets Toxoplasmosis Through Modulating Host Toll-Like Receptor-MyD88 Signaling.Frontiers in immunology · 2021Article
- Astrocytes promote a protective immune response to brain Toxoplasma gondii infection via IL-33-ST2 signaling.PLoS pathogens · 2020Article
- The molecular biology and immune control of chronic Toxoplasma gondii infection.The Journal of clinical investigation · 2020Review
- The immune system utilizes two distinct effector mechanisms of T cells depending on two different life cycle stages of a single pathogen, Toxoplasma gondii, to control its cerebral infection.Parasitology international · 2020Review
- Rotavirus Reprograms Multiple Interferon Receptors and Restricts Their Intestinal Antiviral and Inflammatory Functions.Journal of virology · 2020Article
- Penetration of CD8The American journal of pathology · 2019Article
- PersistentInfection and immunity · 2019Article
- Clonal Deletion of Tumor-Specific T Cells by Interferon-γ Confers Therapeutic Resistance to Combination Immune Checkpoint Blockade.Immunity · 2019Article
- An IFNγ/CXCL2 regulatory pathway determines lesion localization during EAE.Journal of neuroinflammation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We examined the role of interferon-γ (IFN-γ) in expression of chemokine mRNA and proteins in the brain during chronic infection with Toxoplasma gondii using BALB/c and BALB/c-background IFN-γ knockout (IFN-γ(-/-)) mice. BALB/c mice are genetically resistant to development of toxoplasmic encephalitis and establish a latent, chronic infection in the brain through IFN-γ-mediated immune responses. Amounts of mRNA for CXCL9/MIG, CXCL10/IP-10, CXCL11/I-TAC, CCL2/MCP-1, CCL3/MIP-1α, and CCL5/RANTES significantly increased in the brains of wild-type mice after infection. CXCL9/MIG, CXCL10/IP-10, and CCL5/RANTES mRNA were most abundant among these chemokines. An increase in amounts of mRNA for CXCL10/IP-10, CCL2/MCP-1, CCL3/MIP-1α, and CCL5/RANTES was also observed in the brains of IFN-γ(-/-) mice after infection, although CXCL10/I-10 and CCL5/RANTES mRNA levels in infected IFN-γ(-/-) mice were significantly lower than those of infected wild-type animals. Amounts of mRNA for CXCL9/MIG and CXCL11/I-TAC remained at the basal levels in infected IFN-γ(-/-) mice. When amounts of the chemokine proteins were examined in the brain homogenates of uninfected and infected mice of both strains, large amounts of CXCL9/MIG, CXCL10/IP-10, and CCL5/RANTES were detected only in infected wild-type animals. These results indicate that CXCL9/MIG, CXCL10/IP-10, and CCL5/RANTES are the chemokines predominantly induced in the brains of genetically resistant BALB/c mice during chronic infection with T. gondii, and their expression is dependent on IFN-γ.
Indexed as
Identifiers
What OpenQuestion holds
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.