ArticleJournal of immunology (Baltimore, Md. : 1950)2015
T-bet is critical for the development of acute graft-versus-host disease through controlling T cell differentiation and function.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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
29 citing papers in PubMed, 42 citations in OpenAlex.
- Trial
- CD56Haematologica · 2017Trial
- Engineered CD40-biosensor-expressing Treg cells as a cell therapy approach for inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Nanographene Oxide Attenuates Acute GVHD by Modulating Macrophage Polarization in a Xenogeneic Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of CD4Frontiers in cellular and infection microbiology · 2024Review
- Engineering donor lymphocytes with Fas ligand protein effectively prevents acute graft-versus-host disease.Blood advances · 2023Article
- Galectin-3 expression in donor T cells reduces GvHD severity and lethality after allogeneic hematopoietic cell transplantation.Cell reports · 2023Article
- TCF-1 Is Required for CD4 T Cell Persistence Functions during AlloImmunity.International journal of molecular sciences · 2023Article
- Immune surveillance and humoral immune responses in kidney transplantation - A look back at T follicular helper cells.Frontiers in immunology · 2023Review
- The protective and pathogenic role of Th17 cell plasticity and function in the tumor microenvironment.Frontiers in immunology · 2023Review
- Dissecting the regulatory network of transcription factors in T cell phenotype/functioning during GVHD and GVT.Frontiers in immunology · 2023Review
- Early Expression of Functional Markers on CD4Frontiers in immunology · 2022Observational
- Immune Suppression in Allogeneic Hematopoietic Stem Cell Transplantation.Handbook of experimental pharmacology · 2022Article
- LYG1 Deficiency Attenuates the Severity of Acute Graft-Versus-Host DiseaseFrontiers in immunology · 2021Article
- T Cell Subsets in Graft Versus Host Disease and Graft Versus Tumor.Frontiers in immunology · 2021Review
- Granzyme A-producing T helper cells are critical for acute graft-versus-host disease.JCI insight · 2020Article
- Article
- RNA binding protein PCBP1 is an intracellular immune checkpoint for shaping T cell responses in cancer immunity.Science advances · 2020Article
- PRMT5 regulates T cell interferon response and is a target for acute graft-versus-host disease.JCI insight · 2020Article
- [Tole of T cell exhaustion in inducing immune tolerance and preventing graft-versus-host disease].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
T-bet is a master regulator for IFN-γ production and Th1 differentiation. We evaluated the roles of T-bet and IFN-γ in T cell responses in acute graft-versus-host disease (GVHD) and found that T-bet(-/-) T cells induced significantly less GVHD compared with wild-type or IFN-γ(-/-) counterparts in both MHC-mismatched and MHC-matched but minor histocompatibility Ag-mismatched models driven by CD4 T cells. T-bet(-/-), but not IFN-γ(-/-), CD4 T cells had a markedly reduced ability to cause tissue damage in liver and gut. This distinct outcome is reflected by the differential gene expression on donor CD4 T cells deficient for T-bet or IFN-γ. At mRNA and protein levels, we defined several T-bet-dependent molecules that may account for the impaired ability of T-bet(-/-) T cells to migrate into target organs and to produce Th1-related cytokines. Moreover, these molecules were independent of either endogenous IFN-γ, such as CXCR3 and programmed death-1, or systematic IFN-γ, such as NKG2D, I-A(b), and granzyme B. Although both T-bet(-/-) and IFN-γ(-/-) CD4 T cells are prone to differentiate into Th17 cells, polarized Th17 cells deficient for T-bet but not for IFN-γ had a significantly reduced ability to cause GVHD. Finally, T-bet(-/-) T cells had a compromised graft-versus-leukemia effect, which could be essentially reversed by neutralization of IL-17 in the recipients. We conclude that T-bet is required for Th1 differentiation and migration, as well as for optimal function of Th17 cells. Thus, targeting T-bet or regulating its downstream effectors independent of IFN-γ may be a promising strategy to control GVHD in the clinic.
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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.