ArticleMucosal immunology2016
Transforming growth factor-β1 sustains the survival of Foxp3(+) regulatory cells during late phase of oropharyngeal candidiasis infection.
Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
The trial behind it
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Enrichment ofFrontiers in immunology · 2026Article
- Dysbiosis modulates CD8iScience · 2025Article
- Neuroimmune cell interactions and chronic infections in oral cancers.Frontiers in medicine · 2024Article
- Molecular and temporal control of restimulation-induced cell death (RICD) in T lymphocytes.Frontiers in cell death · 2023Article
- Crosstalk between the oral microbiota, mucosal immunity, and the epithelial barrier regulates oral mucosal disease pathogenesis.Mucosal immunology · 2021Review
- Oral immune dysfunction is associated with the expansion of FOXP3Nature communications · 2021Article
- FOXP3 protects conventional human T cells from premature restimulation-induced cell death.Cellular & molecular immunology · 2021Article
- IL-1β-MyD88-mTOR Axis Promotes Immune-Protective IL-17AFrontiers in immunology · 2020Article
- Microbiome Dependent Regulation of TFrontiers in immunology · 2019Review
- FOXP3 renders activated human regulatory T cells resistant to restimulation-induced cell death by suppressing SAP expression.Cellular immunology · 2018Article
- Role of Short Chain Fatty Acids in Controlling TFrontiers in microbiology · 2018Article
- TGF-JCI insight · 2016Article
- Mucosal Regulatory T Cells and T Helper 17 Cells in HIV-Associated Immune Activation.Frontiers in immunology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
As CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) play crucial immunomodulatory roles during infections, one key question is how these cells are controlled during antimicrobial immune responses. Mechanisms controlling their homeostasis are central to ensure efficient protection against pathogens, as well as to control infection-associated immunopathology. Here we studied how their viability is regulated in the context of mouse oropharyngeal candidiasis (OPC) infection, and found that these cells show increased protection from apoptosis during late phase of infection and reinfection. Tregs underwent reduced cell death because they are refractory to T cell receptor restimulation-induced cell death (RICD). We confirmed their resistance to RICD, using mouse and human Tregs in vitro, and by inducing α-CD3 antibody-mediated apoptosis in vivo. The enhanced viability is dependent on increased transforming growth factor-β1 (TGF-β1) signaling that results in upregulation of cFLIP (cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein) in Tregs. Protection from cell death is abrogated in the absence of TGF-β1 signaling in Tregs during OPC infection. Taken together, our data unravel the previously unrecognized role of TGF-β1 in promoting Treg viability, coinciding with the pronounced immunomodulatory role of these cells during later phase of OPC infection, and possibly other mucosal infections.
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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.