ArticleCell death and differentiation2013
A novel subset of helper T cells promotes immune responses by secreting GM-CSF.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 49 citations in OpenAlex.
- Intralymphatic glutamic acid decarboxylase administration in type 1 diabetes patients induced a distinctive early immune response in patients with DR3DQ2 haplotype.Frontiers in immunology · 2023Trial
- Region-specific immune regulation determines differential response to JAK1 inhibition in Crohn's disease ex vivo.Journal of Crohn's & colitis · 2026Article
- Calycosin suppresses the activating effect of granulocyte-macrophage-colony-stimulating factor-producing T helper cells on macrophages in experimental atherosclerosis.Frontiers in pharmacology · 2025Article
- GM-CSFTheranostics · 2025Review
- Physiological and pathogenic T cell autoreactivity converge in type 1 diabetes.Nature communications · 2024Article
- Personalized neoantigen vaccines as early intervention in untreated patients with lymphoplasmacytic lymphoma: a non-randomized phase 1 trial.Nature communications · 2024Article
- Review
- Crosstalk between CD64EMBO molecular medicine · 2024Article
- Review
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia.PLoS pathogens · 2024Article
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract againstbioRxiv : the preprint server for biology · 2023Article
- Dual Functions of T Lymphocytes in Breast Carcinoma: From Immune Protection to Orchestrating Tumor Progression and Metastasis.Cancers · 2023Review
- BAP31 Knockout in Macrophages Affects CD4International journal of molecular sciences · 2023Article
- Next-Generation Adjuvants: Applying Engineering Methods to Create and Evaluate Novel Immunological Responses.Pharmaceutics · 2023Article
- Who Knew? Dopamine Transporter Activity Is Critical in Innate and Adaptive Immune Responses.Cells · 2023Article
- The role of iron metabolism in the pathogenesis and treatment of multiple sclerosis.Frontiers in immunology · 2023Review
- The small molecule inhibitor BX-795 uncouples IL-2 production from inhibition of Th2 inflammation and induces CD4Frontiers in immunology · 2023Article
- Where do T cell subsets stand in SARS-CoV-2 infection: an update.Frontiers in cellular and infection microbiology · 2022Review
- CD4Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A Comprehensive Summary of the Knowledge on COVID-19 Treatment.Aging and disease · 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
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Helper T cells are crucial for maintaining proper immune responses. Yet, they have an undefined relationship with one of the most potent immune stimulatory cytokines, granulocyte macrophage-colony-stimulating factor (GM-CSF). By depleting major cytokines during the differentiation of CD4(+) T cells in vitro, we derived cells that were found to produce large amounts of GM-CSF, but little of the cytokines produced by other helper T subsets. By their secretion of GM-CSF, this novel subset of helper T cells (which we have termed ThGM cells) promoted the production of cytokines by other T-cell subtypes, including type 1 helper T cell (Th1), type 2 helper T cell (Th2), type 1 cytotoxic T cell (Tc1), type 2 cytotoxic T cell (Tc2), and naive T cells, as evidenced by the fact that antibody neutralization of GM-CSF abolished this effect. ThGM cells were found to be highly prone to activation-induced cell death (AICD). Inhibitors of TRAIL or granzymes could not block AICD in ThGM cells, whereas inhibition of FasL/Fas interaction partially rescued ThGM cells from AICD. Thus, ThGM cells are a novel subpopulation of T helper cells that produce abundant GM-CSF, exhibit exquisite susceptibility to apoptosis, and therefore play a pivotal role in the regulation of the early stages of immune responses.
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.