<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu Y</submitter><funding>Yu-Ping Peng</funding><funding>Yi-Hua Qiu</funding><pagination>194</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12532925</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>β2-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.&lt;h4>Methods&lt;/h4>DBA1/J mice were used to prepare CIA model by intradermal injection of collagen type II (CII). Inducible Treg (</pubmed_abstract><journal>Arthritis research &amp; therapy</journal><pubmed_title>Treg cells mitigate inflammatory responses and symptoms via β2-AR/β-Arr2/ERK signaling in an experimental rheumatoid arthritis.</pubmed_title><pmcid>PMC12532925</pmcid><funding_grant_id>31771293</funding_grant_id><funding_grant_id>31371182</funding_grant_id><pubmed_authors>Peng YP</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Lu JH</pubmed_authors><pubmed_authors>Huang HW</pubmed_authors><pubmed_authors>Wang XQ</pubmed_authors><pubmed_authors>Qiu YH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Treg cells mitigate inflammatory responses and symptoms via β2-AR/β-Arr2/ERK signaling in an experimental rheumatoid arthritis.</name><description>&lt;h4>Background&lt;/h4>β2-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.&lt;h4>Methods&lt;/h4>DBA1/J mice were used to prepare CIA model by intradermal injection of collagen type II (CII). Inducible Treg (</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Oct</publication><modification>2026-05-10T03:21:44.747Z</modification><creation>2026-05-10T03:11:17.735Z</creation></dates><accession>S-EPMC12532925</accession><cross_references><pubmed>41107955</pubmed><doi>10.1186/s13075-025-03659-9</doi></cross_references></HashMap>