ArticlePLoS pathogens2021
CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- β-oxidation-mediated differentiation of effector CD4Journal of neuroinflammation · 2026Article
- CXCR6 promotes dermal CD8+ T cell survival and transition to long-term tissue residence.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- CXCR6 promotes dermal CD8bioRxiv : the preprint server for biology · 2025Article
- Article
- Impact of gut microbiota on metabolic dysfunction-associated steatohepatitis and hepatocellular carcinoma: pathways, diagnostic opportunities and therapeutic advances.European journal of medical research · 2024Review
- The CXCL16-CXCR6 axis in glioblastoma modulates T-cell activity in a spatiotemporal context.Frontiers in immunology · 2023Article
- Ontogeny, functions and reprogramming of Kupffer cells upon infectious disease.Frontiers in immunology · 2023Review
- Impact of pulmonary African trypanosomes on the immunology and function of the lung.Nature communications · 2022Article
- The Genomic Profile Associated with Risk of Severe Forms of COVID-19 in Amazonian Native American Populations.Journal of personalized medicine · 2022Article
- Tipping the balance between erythroid cell differentiation and induction of anemia in response to the inflammatory pathology associated with chronic trypanosome infections.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver macrophages internalize circulating bloodborne parasites. It remains poorly understood how this process affects the fate of the macrophages and T cell responses in the liver. Here, we report that infection by Trypanosoma brucei induced depletion of macrophages in the liver, leading to the repopulation of CXCL16-secreting intrahepatic macrophages, associated with substantial accumulation of CXCR6+CD4+ T cells in the liver. Interestingly, disruption of CXCR6 signaling did not affect control of the parasitemia, but significantly enhanced the survival of infected mice, associated with reduced inflammation and liver injury. Infected CXCR6 deficient mice displayed a reduced accumulation of CD4+ T cells in the liver; adoptive transfer experiments suggested that the reduction of CD4+ T cells in the liver was attributed to a cell intrinsic property of CXCR6 deficient CD4+ T cells. Importantly, infected CXCR6 deficient mice receiving wild-type CD4+ T cells survived significantly shorter than those receiving CXCR6 deficient CD4+ T cells, demonstrating that CXCR6+CD4+ T cells promote the mortality. We conclude that infection of T. brucei leads to depletion and repopulation of liver macrophages, associated with a substantial influx of CXCR6+CD4+ T cells that mediates mortality.
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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 Socratic graph.