ArticleInvestigative ophthalmology & visual science2011
CXCL10 is required to maintain T-cell populations and to control parasite replication during chronic ocular toxoplasmosis.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Putative mechanisms of ocular inflammation in syphilis.Journal of ophthalmic inflammation and infection · 2026Review
- Human Retinal Organoid Model of Ocular Toxoplasmosis.Pathogens (Basel, Switzerland) · 2025Article
- Identification of key modules and hub genes for sepsis-induced myopathy using weighted gene co-expression network analysis.Frontiers in genetics · 2025Article
- Modulation of CXCL10 activity as a therapeutic target of ocular toxoplasmosis in diabetic mice.Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2024Article
- Immune Control in RepeatedOpen forum infectious diseases · 2024Article
- Systemic prime exacerbates the ocular immune response to heat-killed Mycobacterium tuberculosis.Experimental eye research · 2022Article
- LFA-1/ ICAM-1 promotes NK cell cytotoxicity associated with the pathogenesis of ocular toxoplasmosis in murine model.PLoS neglected tropical diseases · 2022Article
- Coronavirus Porcine Deltacoronavirus Upregulates MHC Class I Expression through RIG-I/IRF1-Mediated NLRC5 Induction.Journal of virology · 2022Article
- Microglia in CNS infections: insights from Toxoplasma gondii and other pathogens.Trends in parasitology · 2022Review
- Transcriptomic Analysis of the Effects of Chemokine Receptor CXCR3 Deficiency on Immune Responses in the Mouse Brain duringMicroorganisms · 2021Article
- Serum CXCL10/IP-10 may be a potential biomarker for severe Mycoplasma pneumoniae pneumonia in children.BMC infectious diseases · 2021Article
- Treatment Strategy in Human Ocular Toxoplasmosis: Why Antibiotics Have Failed.Journal of clinical medicine · 2021Review
- Murine Model of Primary Acquired Ocular Toxoplasmosis: Fluorescein Angiography and Multiplex Immune Mediator Profiles in the Aqueous Humor.Investigative ophthalmology & visual science · 2021Article
- Lactic acid promotes metastatic niche formation in bone metastasis of colorectal cancer.Cell communication and signaling : CCS · 2021Article
- Article
- Modeling of variables in cellular infection reveals CXCL10 levels are regulated by human genetic variation and the Chlamydia-encoded CPAF protease.Scientific reports · 2020Article
- Head-to-head comparisons of Toxoplasma gondii and its near relative Hammondia hammondi reveal dramatic differences in the host response and effectors with species-specific functions.PLoS pathogens · 2020Article
- Inflammatory and Fibrogenic Factors in Proliferative Vitreoretinopathy Development.Translational vision science & technology · 2020Review
- Global Transcriptome Profiling of Multiple Porcine Organs RevealsFrontiers in immunology · 2019Article
- Immune Mediator Profile in Aqueous Humor Differs in Patients with Primary Acquired Ocular Toxoplasmosis and Recurrent Acute Ocular Toxoplasmosis.Mediators of inflammation · 2019Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeToxoplasma gondii is a major cause of ocular disease, which can lead to permanent vision loss in humans. T cells are critically involved in parasite control, but little is known about the molecules that promote T-cell trafficking and migration in the retina. Thus, the aim of this study was to image and dissect the T-cell response during chronic toxoplasmic retinochoroiditis.
methodsC57BL/6 mice were infected with the Me49 strain of T. gondii, and T cells that infiltrated the eye were analyzed by flow cytometry and imaged using multiphoton microscopy. IFN-γ, CXCL9, CXCL10, and CXCR3 mRNA levels were measured by real-time PCR. To investigate the role of CXCL10, mice were treated with anti-CXCL10 antibodies, and histopathology and immunohistochemistry were performed to monitor changes in pathology, cellular infiltration, and parasite burden in the eye.
resultsInfection with T. gondii leads to the infiltration of highly activated motile T cells into the eye. These cells express CXCR3 and are capable of producing IFN-γ and TNF-α, and CD8+ T cells express granzyme B. The expression of CXCL9 and CXCL10 in the retina was significantly upregulated during chronic infection. Treatment of chronically infected mice with anti-CXCL10 antibodies led to decreases in the numbers of CD3+, CD4+, and CD8+ T cells and the amount of IFN-γ mRNA expression in the retina and an increase in replicating parasites and ocular pathology.
conclusionsThe maintenance of the T-cell response and the control of T. gondii in the eye during chronic infection is dependent on CXCL10.
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