ArticleThe Journal of clinical investigation2018
The vimentin intermediate filament network restrains regulatory T cell suppression of graft-versus-host disease.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- Machine learning-driven decoding of maternal immune signatures in repeated pregnancy loss.PLoS computational biology · 2026Article
- Complement Anaphylatoxin C5a-Induced Mouse Lymphatic Functions Modulate Interactions Between Endothelial Cells and T Lymphocytes.Immune network · 2026Article
- Modulating Vimentin: A Systems-Level Therapeutic Strategy for Sepsis and Complex Diseases.Life (Basel, Switzerland) · 2026Article
- Oral Treatment with the Vimentin-Targeting Compound ALD-R491 Mitigates Hyperinflammation, Multi-Organ Injury, and Mortality in CLP-Induced Septic Mice.Life (Basel, Switzerland) · 2025Article
- Low-dose interleukin-2 induces clonal expansion of BACH2-repressed effector regulatory T cells following acute coronary syndrome.Nature cardiovascular research · 2025Article
- Defining pathogenic IL-17 and CSF-1 gene expression signatures in chronic graft-versus-host disease.Blood · 2025Article
- Vimentin modulates regulatory T cell receptor-ligand interactions at distal pole complex, leading to dysregulated host response to viral pneumonia.Cell reports · 2024Article
- T Cell Resistance: On the Mechanisms of T Cell Non-activation.Immune network · 2024Review
- Intestinal microbiota imbalance resulted by anti-Toxoplasma gondii immune responses aggravate gut and brain injury.Parasites & vectors · 2024Article
- PD1 inhibits PKCθ-dependent phosphorylation of cytoskeleton-related proteins and immune synapse formation.Blood advances · 2024Article
- Tolerating CD47.Clinical and translational medicine · 2024Review
- Transcriptome profiling of regulatory T cells from children with transient hypogammaglobulinemia of infancy.Clinical and experimental immunology · 2023Article
- Vimentin is required for tumor progression and metastasis in a mouse model of non-small cell lung cancer.Oncogene · 2023Article
- Lkb1 loss in regulatory T cells leads to dysregulation of hematopoietic stem cell expansion and differentiation in bone marrow.FEBS open bio · 2023Article
- Roles of vimentin in health and disease.Genes & development · 2022Review
- Emerging translational strategies and challenges for enhancing regulatory T cell therapy for graft-versus-host disease.Frontiers in immunology · 2022Review
- Article
- Article
- Regulatory T Cell Therapy of Graft-versus-Host Disease: Advances and Challenges.International journal of molecular sciences · 2021Review
- Recent Metabolic Advances for Preventing and Treating Acute and Chronic Graft Versus Host Disease.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
26 authors at 8 institutions in 2 countries.
Funding
Abstract
Regulatory T cells (Tregs) are critical for maintaining immune homeostasis. However, current Treg immunotherapies do not optimally treat inflammatory diseases in patients. Understanding the cellular processes that control Treg function may allow for the augmentation of therapeutic efficacy. In contrast to activated conventional T cells, in which protein kinase C-θ (PKC-θ) localizes to the contact point between T cells and antigen-presenting cells, in human and mouse Tregs, PKC-θ localizes to the opposite end of the cell in the distal pole complex (DPC). Here, using a phosphoproteomic screen, we identified the intermediate filament vimentin as a PKC-θ phospho target and show that vimentin forms a DPC superstructure on which PKC-θ accumulates. Treatment of mouse Tregs with either a clinically relevant PKC-θ inhibitor or vimentin siRNA disrupted vimentin and enhanced Treg metabolic and suppressive activity. Moreover, vimentin-disrupted mouse Tregs were significantly better than controls at suppressing alloreactive T cell priming in graft-versus-host disease (GVHD) and GVHD lethality, using a complete MHC-mismatch mouse model of acute GVHD (C57BL/6 donor into BALB/c host). Interestingly, vimentin disruption augmented the suppressor function of PKC-θ-deficient mouse Tregs. This suggests that enhanced Treg activity after PKC-θ inhibition is secondary to effects on vimentin, not just PKC-θ kinase activity inhibition. Our data demonstrate that vimentin is a key metabolic and functional controller of Treg activity and provide proof of principle that disruption of vimentin is a feasible, translationally relevant method to enhance Treg potency.
Indexed as
Identifiers
What OpenQuestion holds
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.