ArticlePLoS biology2022
Endogenously produced catecholamines improve the regulatory function of TLR9-activated B cells.
Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities.Frontiers in physiology · 2026Review
- Dopaminergic signalling in gastrointestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Expansion of B10 cellsInternational journal of molecular medicine · 2025Review
- Adrenergic signaling during parasitic infections.Frontiers in immunology · 2025Review
- Triad3A-Mediated K48-Linked ubiquitination and degradation of TLR9 impairs mitochondrial bioenergetics and exacerbates diabetic cardiomyopathy.Journal of advanced research · 2024Article
- Absence of sympathetic innervation hampers the generation of tertiary lymphoid structures upon acute lung inflammation.Scientific reports · 2024Article
- The cancer-immune dialogue in the context of stress.Nature reviews. Immunology · 2024Review
- [Role of the sympathetic nervous system in chronic inflammation].Zeitschrift fur Rheumatologie · 2023Review
- Anti-Inflammatory Effects of Cannabigerol in Rheumatoid Arthritis Synovial Fibroblasts and Peripheral Blood Mononuclear Cell Cultures Are Partly Mediated by TRPA1.International journal of molecular sciences · 2023Article
- Dopamine, Immunity, and Disease.Pharmacological reviews · 2023Review
- Roles of Mitochondrial DNA Damage in Kidney Diseases: A New Biomarker.International journal of molecular sciences · 2022Review
- Dopamine and norepinephrine are embracing their immune side and so should we.Current opinion in neurobiology · 2022Review
- Article
- β2-Adrenergic Receptor Expression and Intracellular Signaling in B Cells Are Highly Dynamic during Collagen-Induced Arthritis.Biomedicines · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sympathetic nervous system (SNS) contributes to immune balance by promoting anti-inflammatory B cells. However, whether B cells possess a self-regulating mechanism by which they modulate regulatory B cell (Breg) function is not well understood. In this study, we investigated the ability of B cells to synthesize their own catecholamines upon stimulation with different B cell activators and found that expression of the enzyme tyrosine hydroxylase (TH), required to generate catecholamines, is up-regulated by Toll-like receptor (TLR)9. This TLR9-dependent expression of TH correlated with up-regulation of adrenergic receptors (ADRs), enhanced interleukin (IL)-10 production, and overexpression of the co-inhibitory ligands programmed death ligand 1 (PD-L1) and Fas ligand (FasL). Moreover, concomitant stimulation of ß1-3-ADRs together with a B cell receptor (BCR)/TLR9 stimulus clearly enhances the anti-inflammatory potential of Bregs to suppress CD4 T cells, a crucial population in the pathogenesis of autoimmune diseases, like rheumatoid arthritis (RA). Furthermore, TH up-regulation was also demonstrated in B cells during the course of collagen-induced arthritis (CIA), a mouse model for the investigation of RA. In conclusion, our data show that B cells possess an autonomous mechanism to modulate their regulatory function in an autocrine and/or paracrine manner. These findings help to better understand the function of B cells in the regulation of autoimmune diseases and the interplay of SNS.
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