ArticleThe Journal of investigative dermatology2014
β-arrestin 2 inhibits proinflammatory chemokine production and attenuates contact allergic inflammation in the skin.
Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Tissue-resident neutrophils serve homeostatic and immunological functions in embryos.Nature communications · 2026Article
- GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026Review
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- Single-cell transcriptome of retinal myeloid cells in response to transplantation of human neurons reveals reversibility of microglial activation.bioRxiv : the preprint server for biology · 2025Article
- Genome-wide association studies of dairy cattle resistance to digital dermatitis recorded at four distinct lactation stages.Scientific reports · 2025Article
- Identification of Hif1α as a Potential Participant in Autoimmune Uveitis Pathogenesis Using Single-Cell Transcriptome Analysis.Investigative ophthalmology & visual science · 2023Article
- Role of MrgprB2 in Rosacea-Like Inflammation in Mice: Modulation by β-Arrestin 2.The Journal of investigative dermatology · 2022Article
- β2-Adrenergic Receptor Expression and Intracellular Signaling in B Cells Are Highly Dynamic during Collagen-Induced Arthritis.Biomedicines · 2022Article
- MiR-365-3p is a negative regulator in IL-17-mediated asthmatic inflammation.Frontiers in immunology · 2022Article
- β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in macrophages.Bioengineered · 2022Article
- Protective effects of miR-155-5p silencing on IFN-γ-induced apoptosis and inflammation in salivary gland epithelial cells.Experimental and therapeutic medicine · 2021Article
- Multifaceted role of β-arrestins in inflammation and disease.Genes and immunity · 2015Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Arrestins participate in G-protein receptor signaling and act as adapter proteins that direct the recruitment, activation, and scaffolding of various cytoplasmic signaling complexes. β-Arrestin 2-deficient (Arrb2(-/-)) mice show decreased T-cell recruitment into allergic lung tissue but increased neutrophil infiltration into wounded skin. Given these opposing effects in different immune cell subsets, we investigated the role of β-arrestin 2 in the regulation of contact hypersensitivity responses. We observed significantly increased allergic ear swelling to the obligate contact sensitizers DNFB and FITC in Arrb2(-/-) compared with wild-type mice. Immunohistological analyses revealed strikingly increased neutrophil infiltration with abundant subcorneal pustules in inflamed ear tissue of DNFB-allergic Arrb2(-/-) mice. Experiments involving adoptive transfers of sensitized lymphocytes and bone marrow chimeric mice indicated that β-arrestin 2 exerts its anti-inflammatory effects predominantly through radioresistant, skin-resident cells in the challenge phase of contact hypersensitivity. As a potential mechanism, we found that primary cultures of β-arrestin 2-deficient keratinocytes secreted higher levels of neutrophil-attracting chemokines including CXCL1/KC in response to T cell-derived cytokines in vitro. These experimental results support a model in which β-arrestin 2 inhibits the production of proinflammatory chemokines, which limits the recruitment of myeloid immune cells and thereby attenuates allergic skin inflammation.
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