ArticlePLoS pathogens2025
The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Dynamic remodeling of the pancreas immune landscape in obesity.Nature communications · 2026Article
- β-oxidation-mediated differentiation of effector CD4Journal of neuroinflammation · 2026Article
- Divergent Fates of Kidney-Resident Polyomaviruses: Stable Shedding Versus Near-Silent Persistence.Viruses · 2026Article
- Divergent Fates of Kidney-Resident Polyomaviruses: Stable Shedding Versus Near-Silent Persistence.bioRxiv : the preprint server for biology · 2026Article
- Explorative Insights into Local Immune Response to BK Virus-A Cross-Sectional Study in Urine Samples Between Transplant Recipients and Non-Immunocompromised Hosts.Medicina (Kaunas, Lithuania) · 2026Article
- Live long and persist: polyomavirus immune evasion in the brain and kidney.Future virology · 2025Article
- CXCR4 and CXCR6 dually limit T cell entry into the polyomavirus-infected brain.Journal of neuroinflammation · 2025Article
- Shedding dynamics of a DNA virus population during acute and long-term persistent infection.PLoS pathogens · 2025Article
- Combining WGCNA and machine learning to identify mechanisms and biomarkers of hyperthyroidism and atrial fibrillation.Frontiers in cardiovascular medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
BK polyomavirus (PyV) establishes lifelong asymptomatic infections in the reno-urinary system of most humans. BKPyV-associated nephropathy is the leading infectious cause of kidney allograft loss. Using mouse PyV, a natural murine pathogen that also persists in the kidney, we define a dominant chemokine receptor-chemokine axis that directs T cell infiltration of the kidney. We found that CXCR6 was required for CD4+ and CD8+ T cells to be recruited to and retained in the kidney, respectively. Absence of CXCR6 impaired virus control in the kidney. The soluble form of CXCL16 was increased in kidneys of infected mice and in vivo CXCL16 neutralization reduced numbers of virus-specific CD8+ T cells infiltrating the kidney. In vivo administration of IL-12 upregulated CXCR6 expression on virus-specific CD8+ T cells, improved T cell recruitment to the infected kidney, and reduced virus levels. Notably, T cells in kidney biopsies from PyV-associated nephropathy patients express CXCR6 and transcriptional analysis shows significant upregulation of CXCR6 and CXCL16. These findings demonstrate the importance of the CXCR6-CXCL16 axis in regulating T cell responses in the kidney to PyV infection.
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.