ArticleJCI insight2018
Peripheral tissues reprogram CD8+ T cells for pathogenicity during graft-versus-host disease.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- SPHK1 deficiency promotes intestinal homeostasis by ameliorating ER stress-induced gastrointestinal injury during murine graft-versus-host disease.Science China. Life sciences · 2026Article
- Convergent evolution of monocyte differentiation in adult skin instructs Langerhans cell identity.Science immunology · 2024Article
- Article
- Exopolysaccharide-Treated Dendritic Cells Effectively Ameliorate Acute Graft-versus-Host Disease.Transplantation and cellular therapy · 2024Article
- Cross-presenting Langerhans cells are required for the early reactivation of resident CD8Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Impaired expression of metallothioneins contributes to allergen-induced inflammation in patients with atopic dermatitis.Nature communications · 2023Article
- Galectin-3 expression in donor T cells reduces GvHD severity and lethality after allogeneic hematopoietic cell transplantation.Cell reports · 2023Article
- Graft-versus-host disease is locally maintained in target tissues by resident progenitor-like T cells.Immunity · 2023Article
- Complex interactions of cellular players in chronic Graft-versus-Host Disease.Frontiers in immunology · 2023Review
- Loss of T cell tolerance in the skin following immunopathology is linked to failed restoration of the dermal niche by recruited macrophages.Cell reports · 2022Article
- Article
- Spatiotemporal single-cell profiling reveals that invasive and tissue-resident memory donor CD8Science translational medicine · 2021Article
- Granzyme A-producing T helper cells are critical for acute graft-versus-host disease.JCI insight · 2020Article
- Donor monocyte-derived macrophages promote human acute graft-versus-host disease.The Journal of clinical investigation · 2020Article
- Graft-versus-host disease reduces lymph node display of tissue-restricted self-antigens and promotes autoimmunity.The Journal of clinical investigation · 2020Article
- Metabolomics analysis of human acute graft-versus-host disease reveals changes in host and microbiota-derived metabolites.Nature communications · 2019Article
- A wave of monocytes is recruited to replenish the long-term Langerhans cell network after immune injury.Science immunology · 2019Article
- NOTCH and Graft-Versus-Host Disease.Frontiers in immunology · 2018Review
- Unraveling the Mechanisms of Cutaneous Graft-Versus-Host Disease.Frontiers in immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
Graft-versus-host disease (GVHD) is a life-threatening complication of allogeneic stem cell transplantation induced by the influx of donor-derived effector T cells (TE) into peripheral tissues. Current treatment strategies rely on targeting systemic T cells; however, the precise location and nature of instructions that program TE to become pathogenic and trigger injury are unknown. We therefore used weighted gene coexpression network analysis to construct an unbiased spatial map of TE differentiation during the evolution of GVHD and identified wide variation in effector programs in mice and humans according to location. Idiosyncrasy of effector programming in affected organs did not result from variation in T cell receptor repertoire or the selection of optimally activated TE. Instead, TE were reprogrammed by tissue-autonomous mechanisms in target organs for site-specific proinflammatory functions that were highly divergent from those primed in lymph nodes. In the skin, we combined the correlation-based network with a module-based differential expression analysis and showed that Langerhans cells provided in situ instructions for a Notch-dependent T cell gene cluster critical for triggering local injury. Thus, the principal determinant of TE pathogenicity in GVHD is the final destination, highlighting the need for target organ-specific approaches to block immunopathology while avoiding global immune suppression.
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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.