ReviewJournal of inflammation research2025
Emerging Role and Function of Th9 Cells in Allergic Inflammation.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.Frontiers in immunology · 2026Review
- Interplay between microRNAs and TGF-β signaling in T cells: implications for Th9 differentiation and immune pathogenesis.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Th9 cells have emerged as pivotal orchestrators of allergic inflammation across the airway, skin, and nasal mucosa, constituting a mechanistically distinct axis beyond canonical Th2 immunity. This review specifically highlights: (i) the Th9 axis as a unifying driver in asthma, atopic dermatitis, and allergic rhinitis; (ii) key mechanistic programs, including signal transducer and activator of transcription (STAT) 5/STAT6 licensing of the IL9 locus, peroxisome proliferator-activated receptor (PPAR) γ-mammalian target of rapamycin complex (mTORC) 1 metabolic wiring, and the IL-9-monocarboxylate transporter (MCT) 1 feedback loop; (iii) organ-level phenotypes such as eosinophil-independent bronchial hyperresponsiveness (BHR) and variable steroid responsiveness; and (iv) therapeutic implications, including biomarker-guided endotyping, Janus kinase (JAK) inhibition, TNF-like ligand (TL) 1A/death receptor (DR) 3 blockade, and metabolic or airway smooth muscle (ASM) tone modulation. Differentiating under the combined influence of interleukin (IL)‑4 and tumor growth factor (TGF)-β, Th9 cells secrete IL‑9, a pleiotropic cytokine that drives mast‑cell proliferation, goblet cell metaplasia, and airway remodeling. Their transcriptional program is epigenetically licensed by STAT5/STAT6, which opens chromatin at the
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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.