ArticleCell research2014
STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation.
Article in Cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 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
114 citing papers in PubMed, 198 citations in OpenAlex.
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- The 2025 Nobel Prize in Physiology or Medicine: The Treg, FoxP3, and STAT-regulated immune network.hLife · 2025Article
- Exposure to Dietary Nitrite Exacerbates Lupus in MRL/lpr Mice by Enhancing Integrin Alpha M.Inflammation · 2025Article
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- Remote Ischemic Post-conditioning Reduces Cognitive Impairment in Rats Following Subarachnoid Hemorrhage: Possible Involvement in STAT3/STAT5 Phosphorylation and Th17/Treg Cell Homeostasis.Translational stroke research · 2025Article
- Novel insights into the ROCK-JAK-STAT signaling pathway in upper respiratory tract infections and neurodegenerative diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Emerging Therapeutic Targets in Rheumatoid Arthritis: Focusing on HIF-1α, Nrf2, STATs, and RORγt.Current drug targets · 2025Review
- GM-CSFTheranostics · 2025Review
- GM-CSF production by immune cells in steady state and autoimmune neuroinflammation mapped using fate reporting mice.Frontiers in immunology · 2025Article
- IL-12 and GM-CSF engineered dendritic cells enhance the enrichment and selection of tumor-reactive T cells for cancer immunotherapy.Frontiers in immunology · 2025Article
- Calycosin suppresses the activating effect of granulocyte-macrophage-colony-stimulating factor-producing T helper cells on macrophages in experimental atherosclerosis.Frontiers in pharmacology · 2025Article
- NKp46Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- T Helper Cells Producing Granulocyte-Macrophage Colony Stimulating Factor as a Risk Marker for Coronary Heart Disease.Bulletin of experimental biology and medicine · 2024Article
- Review
- Targeting of STAT5 using the small molecule topotecan hydrochloride suppresses acute myeloid leukemia progression.Oncology reports · 2023Article
- JAK-STAT signaling in inflammation and stress-related diseases: implications for therapeutic interventions.Molecular biomedicine · 2023Review
- JAK inhibition ameliorated experimental autoimmune encephalomyelitis by blocking GM-CSF-driven inflammatory signature of monocytes.Acta pharmaceutica Sinica. B · 2023Article
- Evolving cognition of the JAK-STAT signaling pathway: autoimmune disorders and cancer.Signal transduction and targeted therapy · 2023Review
- The Significance of SPP1 in Lung Cancers and Its Impact as a Marker for Protumor Tumor-Associated Macrophages.Cancers · 2023Review
- Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis.Cell death and differentiation · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
T helper (TH)-cell subsets, such as TH1 and TH17, mediate inflammation in both peripheral tissues and central nervous system. Here we show that STAT5 is required for T helper-cell pathogenicity in autoimmune neuroinflammation but not in experimental colitis. Although STAT5 promotes regulatory T cell generation and immune suppression, loss of STAT5 in CD4+ T cells resulted in diminished development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Our results showed that loss of encephalitogenic activity of STAT5-deficient autoreactive CD4+ T cells was independent of IFN-γ or interleukin 17 (IL-17) production, but was due to the impaired expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), a crucial mediator of T-cell pathogenicity. We further showed that IL-7-activated STAT5 promotes the generation of GM-CSF-producing CD4+ T cells, which were preferentially able to induce more severe EAE than TH17 or TH1 cells. Consistent with GM-CSF-producing cells being a distinct subset of TH cells, the differentiation program of these cells was distinct from that of TH17 or TH1 cells. We further found that IL-3 was secreted in a similar pattern as GM-CSF in this subset of TH cells. In conclusion, the IL-7-STAT5 axis promotes the generation of GM-CSF/IL-3-producing TH cells. These cells display a distinct transcriptional profile and may represent a novel subset of T helper cells which we designate as TH-GM.
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.