ArticleJournal of leukocyte biology2025
Cxcl10 is protective during mouse-adapted SARS-CoV-2 infection.
Article in Journal of leukocyte biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Characterization of an isogenicInfection and immunity · 2026Article
- SARS-CoV-2 virus infection ofbioRxiv : the preprint server for biology · 2026Article
- CXCR3 ameliorates neutrophil-dependent disease severity in SARS-CoV-2 infection by regulating CD4Frontiers in immunology · 2026Article
- Membrane Protein of SARS-CoV-2 Promotes the Production of CXCL10 and Apoptosis of Myocardial Cells.Cardiovascular toxicology · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of the coronavirus disease 2019 (COVID-19) pandemic, remains endemic worldwide. Circulating levels of the chemokine CXCL10 are strongly positively associated with poor outcome; however, its precise role in SARS-CoV-2 pathogenesis and its suitability as a therapeutic target have remained undefined. Here, we challenged mice genetically deficient in Cxcl10 with a mouse-adapted strain of SARS-CoV-2. Infected male, but not female, Cxcl10-/- mice displayed increased mortality compared to wild type controls. Histopathological damage, inflammatory gene induction, and virus load in the lungs of male mice were not broadly influenced by Cxcl10 deficiency. However, accumulation of B and T lymphocytes in the lung parenchyma of infected mice was reduced in the absence of Cxcl10. Thus, during acute SARS-CoV-2 infection, Cxcl10 regulates lymphocyte infiltration in lung and confers protection against mortality. Our preclinical model results do not support targeting CXCL10 therapeutically in severe COVID-19.
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