ArticleEuropean journal of immunology2008
CXCR3-deficiency protects influenza-infected CCR5-deficient mice from mortality.
Article in European journal of immunology, 2008. 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, 62 citations in OpenAlex.
- Airway macrophage specific glycocalyx expression and remodeling following viral infection.Matrix biology : journal of the International Society for Matrix Biology · 2026Article
- B cell-intrinsic CXCR3 drives efficient generation of ectopic pulmonary germinal center responses to influenza A virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The chemokine receptor CXCR3 promotes CD8Science advances · 2024Article
- IL-4/IL-4 Ab complex enhances the accumulation of both antigen-specific and bystander CD8 T cells in mouse lungs infected with influenza A virus.Laboratory animal research · 2023Article
- T cell-specific P2RX7 favors lung parenchymal CD4Cell reports · 2023Article
- Quantitative analyses of T cell motion in tissue reveals factors driving T cell search in tissues.eLife · 2023Article
- CXCR3 Provides a Competitive Advantage for Retention ofVaccines · 2023Article
- The CXCL10/CXCR3 Axis Promotes Disease Pathogenesis in Mice upon CVA2 Infection.Microbiology spectrum · 2022Article
- Comparison of Lung-Homing Receptor Expression and Activation Profiles on NK Cell and T Cell Subsets in COVID-19 and Influenza.Frontiers in immunology · 2022Article
- Profound dysregulation of T cell homeostasis and function in patients with severe COVID-19.Allergy · 2021Article
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Antibody-suppressor CD8+ T Cells Require CXCR5.Transplantation · 2019Article
- Neutrophils Induce a Novel Chemokine Receptors Repertoire During Influenza Pneumonia.Frontiers in cellular and infection microbiology · 2019Article
- CXCR6-Deficiency Improves the Control of PulmonaryFrontiers in immunology · 2019Article
- Chemokines: Critical Regulators of Memory T Cell Development, Maintenance, and Function.Advances in immunology · 2018Review
- Type 1 Conventional CD103Frontiers in immunology · 2018Article
- Natural Killer Cell Recruitment to the Lung During Influenza A Virus Infection Is Dependent on CXCR3, CCR5, and Virus Exposure Dose.Frontiers in immunology · 2018Article
- TGF-β Controls the Formation of Kidney-Resident T Cells via Promoting Effector T Cell Extravasation.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- In vivo Ebola virus infection leads to a strong innate response in circulating immune cells.BMC genomics · 2016Article
- CCR5 ameliorates Japanese encephalitis via dictating the equilibrium of regulatory CD4(+)Foxp3(+) T and IL-17(+)CD4(+) Th17 cells.Journal of neuroinflammation · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mice lacking the chemokine receptor CCR5 are susceptible to mortality from a normally non-lethal influenza infection. Here we found that CXCR3-deficiency rescued CCR5-deficient (CCR5(-/-)) mice from influenza-induced mortality. The number of mononuclear phagocytes in the airways was transiently increased in CCR5(-/-) mice but not in CXCR3-CCR5 double-deficient mice. Antigen-specific CXCR3-CCR5 double-deficient CD8 effector cells were less efficient at entering the airways compared with WT or CCR5(-/-) CD8 effector cells. The decrease in inflammatory cell infiltrates in CXCR3-CCR5 double-deficient-infected mice correlated with a decrease in CCL2 and IFN-gamma production in the airways. Finally, CXCR3-CCR5 double-deficient mice that survived the primary viral challenge were protected from a lethal secondary challenge, indicating that T-cell-mediated protective memory was not compromised in mice lacking these chemokine receptors. In conclusion, CXCR3-deficiency attenuated the lethal cellular immune response in CCR5(-/-) influenza-infected mice without hindering viral clearance or long-term immunity.
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.