ArticleJournal of immunology (Baltimore, Md. : 1950)2013
γδ T cells are essential effectors of type 1 diabetes in the nonobese diabetic mouse model.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- Similarities and singularities between innate-like T cell subsets in adults with type 1 diabetes.iScience · 2026Article
- Harnessing the potential of γδ T cells through engineering and combination treatment for cancer therapies.Nature communications · 2026Review
- Gluten-Free Diet Induces Small-Scale Changes Across Multiple T-Cell Subsets in NOD Mice.European journal of immunology · 2025Article
- Intestinal mucosal immunity and type 1 diabetes: Non-negligible communication between gut and pancreas.Diabetes, obesity & metabolism · 2025Review
- Identification and Validation of Tryptophan Metabolism-Related Genes in Diabetic Kidney Disease and Construction of a Clinical Prediction Model.Journal of diabetes research · 2025Article
- γδ T cells in diabetes mellitus: dual roles and therapeutic implications.Frontiers in immunology · 2025Review
- Heterozygous BTNL8 variants in individuals with multisystem inflammatory syndrome in children (MIS-C).The Journal of experimental medicine · 2024Article
- The Role of Gamma Delta T Lymphocytes in Physiological and Pathological Condition-Focus on Psoriasis, Atopic Dermatitis, Autoimmune Disorders, Cancer and Lymphomas.International journal of molecular sciences · 2024Review
- Lkb1 orchestrates γδ T-cell metabolic and functional fitness to control IL-17-mediated autoimmune hepatitis.Cellular & molecular immunology · 2024Article
- Intraepithelial Lymphocytes of the Intestine.Annual review of immunology · 2024Review
- Mechanisms governing bystander activation of T cells.Frontiers in immunology · 2024Review
- Adolescent alcohol drinking interaction with the gut microbiome: implications for adult alcohol use disorder.Advances in drug and alcohol research · 2024Article
- γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023Review
- The human Stat1 gain-of-function T385M mutation causes expansion of activated T-follicular helper/T-helper 1-like CD4 T cells and sex-biased autoimmunity in specific pathogen-free mice.Frontiers in immunology · 2023Article
- Development of γδ T Cells: Soldiers on the Front Lines of Immune Battles.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Exploring the potential mechanisms of Tongmai Jiangtang capsules in treating diabetic nephropathy through multi-dimensional data.Frontiers in endocrinology · 2023Article
- Mass cytometry reveals the corneal immune cell changes at single cell level in diabetic mice.Frontiers in endocrinology · 2023Article
- T cells and their products in diabetic kidney disease.Frontiers in immunology · 2023Review
- TOX deficiency facilitates the differentiation of IL-17A-producing γδ T cells to drive autoimmune hepatitis.Cellular & molecular immunology · 2022Article
- A Distinctive γδ T Cell Repertoire in NOD Mice Weakens Immune Regulation and Favors Diabetic Disease.Biomolecules · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
γδ T cells, a lineage of innate-like lymphocytes, are distinguished from conventional αβ T cells in their Ag recognition, cell activation requirements, and effector functions. γδ T cells have been implicated in the pathology of several human autoimmune and inflammatory diseases and their corresponding mouse models, but their specific roles in these diseases have not been elucidated. We report that γδ TCR(+) cells, including both the CD27(-)CD44(hi) and CD27(+)CD44(lo) subsets, infiltrate islets of prediabetic NOD mice. Moreover, NOD CD27(-)CD44(hi) and CD27(+)CD44(lo) γδ T cells were preprogrammed to secrete IL-17, or IFN-γ upon activation. Adoptive transfer of type 1 diabetes (T1D) to T and B lymphocyte-deficient NOD recipients was greatly potentiated when γδ T cells, and specifically the CD27(-) γδ T cell subset, were included compared with transfer of αβ T cells alone. Ab-mediated blockade of IL-17 prevented T1D transfer in this setting. Moreover, introgression of genetic Tcrd deficiency onto the NOD background provided robust T1D protection, supporting a nonredundant, pathogenic role of γδ T cells in this model. The potent contributions of CD27(-) γδ T cells and IL-17 to islet inflammation and diabetes reported in this study suggest that these mechanisms may also underlie human T1D.
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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.