ArticleArthritis research & therapy2025
Treg cells mitigate inflammatory responses and symptoms via β2-AR/β-Arr2/ERK signaling in an experimental rheumatoid arthritis.
Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Targeting β2-Adrenergic Receptor Stability With Lycorine Reveals a Host-Directed Pathway for Antiviral Defense Against Poxviruses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hyaluronic acid microneedle patch for transdermal delivery of naringin-loaded PEGylated terpesomes in a rat model of rheumatoid arthritis: Modulation TGF-β1, oxidative stress, and inflammation.International journal of pharmaceutics: X · 2026Article
- Shared diagnostic biomarkers in metabolic syndrome and coronary artery disease identified by integrated bioinformatics and machine learning.Endocrine connections · 2026Article
- Roles of gut metabolites on bone mineralization and remodeling: impact of metabolic dysregulation on the gut-immune-bone axis.Frontiers in endocrinology · 2026Review
- Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities.Frontiers in physiology · 2026Review
- Research Progress of Molecular HDrug design, development and therapy · 2026Review
- Article
- Soluble IL-2 receptor and memory Treg profiles differentiate early rheumatoid arthritis from undifferentiated arthritis at initial presentation.Frontiers in immunology · 2026Article
- MIS-C pathogenesis: immune dysregulation & viral triggers.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundβ2-adrenergic receptor (β2-AR) is widely expressed on immune cells, including T cells and it has a non-canonical signaling pathway, which is β2-AR-β-arrestin 2 (β-Arr2)-extracellular signal-regulated kinase 1/2 (ERK1/2). Our previous studies have shown that the β2-AR agonist terbutaline (Terb) can activate β2-AR and significantly inhibit helper T (Th) 17 cell function in collagen-induced arthritis (CIA). However, the effects of β2-AR on regulatory T (Treg) cells in CIA have not been consistently determined. The aim of our research was to explore whether β2-AR-β-Arr2-ERK1/2 signaling in Treg cells regulates inflammatory responses and signs in CIA.
methodsDBA1/J mice were used to prepare CIA model by intradermal injection of collagen type II (CII). Inducible Treg (iTreg) cells were induced from CD4
resultsThe increased β-Arr2 expression and pERK1/2 level induced by Terb in CIA iTregs were reduced by β-Arr2 gene silence. The increased TGF-β and IL-10 production in iTreg cells by Terb and the suppression of Teff cell proliferation mediated by Terb-treated nTregs from CIA mice were downregulated by β-Arr2 gene silence or U0126 and further enhanced by β-Arr2 gene overexpression. Adoptive transfer of β-Arr2-overexpressed Treg cells into CIA mice reduced limb inflammation, osteoclast-specific gene expression in joints and Th17 cell cytokine production in joints and serum but increased osteoblast-specific gene expression in joints and Treg cell cytokine production in joints and serum.
conclusionsβ2-AR/β-Arr2/ERK signaling in Treg cells contributes to alleviation of inflammatory responses and symptoms in CIA.
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