ArticleScientific reports2025
Single cell analysis identifies distinct CD4 + T cells associated with the pathobiology of pediatric obesity related asthma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Comparative response to pharmacological management of asthma in overweight/obese childrenEuropean respiratory review : an official journal of the European Respiratory Society · 2026Pooled it
- T cell dysregulation and remodeling in pediatric obesity and weight loss.bioRxiv : the preprint server for biology · 2026Article
- Inflammatory Dysregulation, Asthma, and Obesity in Children: What is the Relationship?Journal of inflammation research · 2026Review
- Lung NR3C1Communications biology · 2025Article
- Identifying the Genetic Ancestry of the Pediatric Obesity-Related Asthma Variant (rs6494395) at Rps27l.Pediatric pulmonology · 2025Article
- A Prognostic Nomogram Based on an Immunogenic Cell Death and Endoplasmic Reticulum Stress-Related Gene Signature for Ovarian Cancer.International journal of women's health · 2025Article
- Current state of cancer immunity cycle: new strategies and challenges of using precision hydrogels to treat breast cancer.Frontiers in immunology · 2025Review
- Single-Cell Analysis: A Method for In-Depth Phenotyping of Cells Involved in Asthma.International journal of molecular sciences · 2024Review
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Abstract
Pediatric obesity-related asthma is characterized by non-atopic T helper 1 (Th1) inflammation and steroid resistance. CDC42 upregulation in CD4 + T cells underlies Th1 inflammation but the CD4 + T cell subtype(s) with CDC42 upregulation and their contribution to steroid resistance are not known. Compared to healthy-weight asthma, obesity-alone and healthy-weight controls, single-cell transcriptomics of obese asthma CD4 + T cells revealed CDC42 upregulation in 3 clusters comprised of naïve and central memory T cells, which differed from the cluster enriched for Th1 responses that was comprised of effector T cells. NR3C1, coding for the glucocorticoid receptor, was downregulated, while genes coding for NLRP3 inflammasome were upregulated, in clusters with CDC42 upregulation and Th1 responses. Conserved genes in these clusters correlated with pulmonary function deficits in obese asthma. These findings suggest that several distinct CD4 + T cell subtypes are programmed in obese asthma for CDC42 upregulation, Th1 inflammation, and steroid resistance, and together contribute to the obese asthma phenotype.
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