ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
Multiomics Analysis Identifies SOCS1 as Restraining T Cell Activation and Preventing Graft-Versus-Host Disease.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Randomized trial of anti-thymocyte globulin plus lowdose post-transplant cyclophosphamide to prevent graft-Haematologica · 2025Trial
- Immune reset: what do we learn from bone marrow transplantation.Medical review (2021) · 2026Review
- Enhancing persistence while managing cytokine release syndrome to embrace next-generation CAR-T cell therapy.Journal of translational medicine · 2026Review
- Loss of SOCS1 in Donor T Cells Exacerbates Intestinal GVHD by Driving a Chemokine-Dependent Pro-Inflammatory Immune Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gastrointestinal acute graft versus host disease: a translational perspective from pathogenesis to precision prevention and treatment.Frontiers in immunology · 2026Review
- Aberrant STAT3 activation and overproduction of IL-21 in systemic lupus erythematosus: role of miR-155 and miR-21 in target genesFrontiers in immunology · 2026Article
- Single-cell RNA sequencing reveals heterogeneity of mucosaassociated invariant T cells in donor grafts and its diagnostic relevance in gastrointestinal graft-Haematologica · 2026Article
- T Cell immune reconstitution after allo-HSCT: key factors and implications.Blood science (Baltimore, Md.) · 2025Review
- Immunoregulatory Microenvironment in the Elderly Skin.JID innovations : skin science from molecules to population health · 2025Article
- Multi-omics integration analysis identifies INPP4B as a T-cell-specific activation suppressor.Clinical and translational medicine · 2025Article
- A donor PD-1Signal transduction and targeted therapy · 2025Article
- Optimization of T-cell-replete haploidentical hematopoietic stem cell transplantation: the Chinese experience.Haematologica · 2025Review
- M1 Macrophage is a Novel Potential Trigger for Endothelial Senescence: Role of Exosomal miR-155 Targeting SOCS1 Signal.Human mutation · 2025Article
- Multiomics Integration and Machine Learning Reveal Colony Stimulating Factor 3 Receptor as a Key Gene and Therapeutic Target in Crohn's Disease.Mediators of inflammation · 2025Article
- Ferroptosis-related gene signature-based subtype identification of triple-negative breast cancer to prioritize treatment strategies.Frontiers in oncology · 2025Article
- MicroRNA-155 targets SOCS1 to inhibit osteoclast differentiation during orthodontic tooth movement.BMC oral health · 2023Article
- Development of allogeneic hematopoietic stem cell transplantation in 2022: Regenerating "Groot" to heal the world.Innovation (Cambridge (Mass.)) · 2023Review
- Multiomics Analysis Identifies SOCS1 as Restraining T Cell Activation and Preventing Graft-Versus-Host Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Graft-versus-host disease (GVHD) is a major life-threatening complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Inflammatory signaling pathways promote T-cell activation and are involved in the pathogenesis of GVHD. Suppressor of cytokine signaling 1 (SOCS1) is a critical negative regulator for several inflammatory cytokines. However, its regulatory role in T-cell activation and GVHD has not been elucidated. Multiomics analysis of the transcriptome and chromatin structure of granulocyte-colony-stimulating-factor (G-CSF)-administered hyporesponsive T cells from healthy donors reveal that G-CSF upregulates SOCS1 by reorganizing the chromatin structure around the SOCS1 locus. Parallel in vitro and in vivo analyses demonstrate that SOCS1 is critical for restraining T cell activation. Loss of Socs1 in T cells exacerbates GVHD pathogenesis and diminishes the protective role of G-CSF in GVHD mouse models. Further analysis shows that SOCS1 inhibits T cell activation not only by inhibiting the colony-stimulating-factor 3 receptor (CSF3R)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway, but also by restraining activation of the inflammasome signaling pathway. Moreover, high expression of SOCS1 in T cells from patients correlates with low acute GVHD occurrence after HSCT. Overall, these findings identify that SOCS1 is critical for inhibiting T cell activation and represents a potential target for the attenuation of GVHD.
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