ArticleJCI insight2022
STAT1 signaling protects self-reactive T cells from control by innate cells during neuroinflammation.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Adipocyte-derived LTB4 programs human NKG2AJournal for immunotherapy of cancer · 2026Article
- Causal Relationship Between Circulating Leukocyte Characteristics and Immune Cell Traits With Multiple Sclerosis Risk: A Two-Sample Bidirectional Mendelian Randomisation Study.Cellular and molecular neurobiology · 2026Article
- Article
- Integrin CD103 expression in naive CD8Immunity · 2025Article
- Bulk RNAseq Analysis of Cardiac Myosin-Specific CD4Biomedicines · 2025Article
- Defining a novel DYRK1A-gp130/IL-6R-pSTAT axis that regulates Th17 differentiation.ImmunoHorizons · 2025Article
- Single-Cell Transcriptomics Uncover EEF1A1-Driven Ubiquitination Dysregulation in T Cell Exhaustion and SLE Pathogenesis via STAT1-Mediated Th1/Th2 Imbalance.Mediators of inflammation · 2025Article
- Distinct baseline immune characteristics associated with responses to conjugated and unconjugated pneumococcal polysaccharide vaccines in older adults.Nature immunology · 2024Article
- STAT1 Employs Myeloid Cell-Extrinsic Mechanisms to Regulate the Neutrophil Response and Provide Protection against Invasive Klebsiella pneumoniae Lung Infection.ImmunoHorizons · 2024Article
- STAT1 Controls the Functionality of Influenza-Primed CD4 T Cells but Therapeutic STAT4 Engagement Maximizes Their Antiviral Impact.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- T cell intrinsic STAT1 signaling prevents aberrant Th1 responses during acute toxoplasmosis.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor STAT1 plays a critical role in modulating the differentiation of CD4+ T cells producing IL-17 and GM-CSF, which promote the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). The protective role of STAT1 in MS and EAE has been largely attributed to its ability to limit pathogenic Th cells and promote Tregs. Using mice with selective deletion of STAT1 in T cells (STAT1CD4-Cre), we identified a potentially novel mechanism by which STAT1 regulates neuroinflammation independently of Foxp3+ Tregs. STAT1-deficient effector T cells became the target of NK cell-mediated killing, limiting their capacity to induce EAE. STAT1-deficient T cells promoted their own killing by producing more IL-2 that, in return, activated NK cells. Elimination of NK cells restored EAE susceptibility in STAT1CD4-Cre mice. Therefore, our study suggests that the STAT1 pathway can be manipulated to limit autoreactive T cells during autoimmunity directed against the CNS.
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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.