ArticleImmunity2013
The inhibitory receptor BTLA controls γδ T cell homeostasis and inflammatory responses.
Article in Immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
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.
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Who cites it
55 citing papers in PubMed, 91 citations in OpenAlex.
- A temporal differentiation program after birth delineates γδ T cell immunity.Science advances · 2026Article
- Dynamics of checkpoint receptors in γδ T cell subsets are associated with clinical response during anti-PD-1 immunotherapies.EMBO molecular medicine · 2026Article
- MutantFrontiers in immunology · 2026Article
- Review
- Innovative Therapies Targeting Drug-Resistant Biomarkers in Metastatic Clear Cell Renal Cell Carcinoma (ccRCC).International journal of molecular sciences · 2024Review
- BTLA contributes to acute-on-chronic liver failure infection and mortality through CD4Nature communications · 2024Article
- Identification of Diagnostic Genes of Aortic Stenosis That Progresses from Aortic Valve Sclerosis.Journal of inflammation research · 2024Article
- γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023Review
- Epitope topography of agonist antibodies to the checkpoint inhibitory receptor BTLA.Structure (London, England : 1993) · 2023Article
- Article
- PD-1 and TIM-3 differentially regulate subsets of mouse IL-17A-producing γδ T cells.The Journal of experimental medicine · 2023Article
- Btla signaling in conventional and regulatory lymphocytes coordinately tempers humoral immunity in the intestinal mucosa.Cell reports · 2022Article
- Comparison of Immune Checkpoint MoleculesBrain sciences · 2022Article
- Releasing the restraints of Vγ9Vδ2 T-cells in cancer immunotherapy.Frontiers in immunology · 2022Article
- Interleukin-10 improves stroke outcome by controlling the detrimental Interleukin-17A response.Journal of neuroinflammation · 2021Article
- Inhibiting the Unconventionals: Importance of Immune Checkpoint Receptors in γδ T, MAIT, and NKT Cells.Cancers · 2021Review
- Immune Checkpoints in Pediatric Solid Tumors: Targetable Pathways for Advanced Therapeutic Purposes.Cells · 2021Review
- Novel human immunomodulatory T cell receptors and their double-edged potential in autoimmunity, cardiovascular disease and cancer.Cellular & molecular immunology · 2021Review
- The BTLA and PD-1 signaling pathways independently regulate the proliferation and cytotoxicity of human peripheral blood γδ T cells.Immunity, inflammation and disease · 2021Article
- Soluble B7-CD28 Family Inhibitory Immune Checkpoint Proteins and Anti-Cancer Immunotherapy.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
γδ T cells rapidly secrete inflammatory cytokines at barrier sites that aid in protection from pathogens, but mechanisms limiting inflammatory damage remain unclear. We found that retinoid-related orphan receptor gamma-t (RORγt) and interleukin-7 (IL-7) influence γδ T cell homeostasis and function by regulating expression of the inhibitory receptor, B and T lymphocyte attenuator (BTLA). The transcription factor RORγt, via its activating function-2 domain, repressed Btla transcription, whereas IL-7 increased BTLA levels on the cell surface. BTLA expression limited γδ T cell numbers and sustained normal γδ T cell subset frequencies by restricting IL-7 responsiveness and expansion of the CD27(-)RORγt(+) population. BTLA also negatively regulated IL-17 and TNF production in CD27(-) γδ T cells. Consequently, BTLA-deficient mice exhibit enhanced disease in a γδ T cell-dependent model of dermatitis, whereas BTLA agonism reduced inflammation. Therefore, by coordinating expression of BTLA, RORγt and IL-7 balance suppressive and activation stimuli to regulate γδ T cell homeostasis and inflammatory responses.
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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 OpenQuestion graph.