ArticlePloS one2012
β1-Adrenoceptor autoantibodies from DCM patients enhance the proliferation of T lymphocytes through the β1-AR/cAMP/PKA and p38 MAPK pathways.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 58 citations in OpenAlex.
- Myocardial Recovery in Patients With Systolic Heart Failure and Autoantibodies Against βJournal of the American College of Cardiology · 2017Trial
- β-Adrenergic receptors as immunomodulators in T cells: mechanisms of neuroimmune crosstalk and pathophysiological implications.Molecular medicine (Cambridge, Mass.) · 2026Review
- A Novel Study of β1- and β2-Adrenergic Receptors Present on PBMCs, T Cells, Monocytes, and NK Cells by Radioligand Method: Quantitation and Correlations.International journal of molecular sciences · 2025Article
- Associations between functional autoantibodies targeting GPCRs, antinuclear antibodies, and inflammatory cytokines TNF-α: a cross-sectional study of 19,810 individuals.Frontiers in immunology · 2025Article
- CTLA-4 silencing could promote anti-tumor effects in hepatocellular.Medical oncology (Northwood, London, England) · 2024Article
- Modulation of cAMP/cGMP signaling as prevention of congenital heart defects in Pde2A deficient embryos: a matter of oxidative stress.Cell death & disease · 2024Article
- βJournal of cardiovascular development and disease · 2023Review
- Clinical and prognostic associations of autoantibodies recognizing adrenergic/muscarinic receptors in patients with heart failure.Cardiovascular research · 2023Article
- The Molecular Role of Immune Cells in Dilated Cardiomyopathy.Medicina (Kaunas, Lithuania) · 2023Review
- Low-level tragus stimulation improves autoantibody-induced hyperadrenergic postural tachycardia syndrome in rabbits.Heart rhythm O2 · 2023Article
- Internal Transcribed Spacer (ITS) Region of Nuclear Ribosomal DNA as a Suitable DNA Barcode for Identification of Zanthoxylum armatum DC. from Manipur.Molecular biotechnology · 2022Article
- Macrophage polarization is involved in liver fibrosis induced by βActa biochimica et biophysica Sinica · 2022Article
- The abnormal distribution of peripheral B1 cells and transition B cells in patients with idiopathic dilated cardiomyopathy: a pilot study.BMC cardiovascular disorders · 2022Article
- Adiponectin up-regulates the decrease of myocardial autophagic flux induced by βJournal of cellular and molecular medicine · 2021Article
- Sex Differences, Genetic and Environmental Influences on Dilated Cardiomyopathy.Journal of clinical medicine · 2021Review
- Diagnostic and prognostic value of autoantibodies against βExperimental and therapeutic medicine · 2020Article
- Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II.Frontiers in physiology · 2020Article
- Cyclic peptide RD808 reduces myocardial injury induced by βHeart and vessels · 2019Article
- Autoantibodies Against βJournal of the American Heart Association · 2019Article
- Autoantibody against βCell death & disease · 2019Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutoantibodies against the second extracellular loop of the β(1)-adrenergic receptor (β(1)-AA) not only contribute to increased susceptibility to heart failure, but also play a causative role in myocardial remodeling through their sympathomimetic-like effects that are induced upon binding to the β(1)-adrenergic receptor. However, their role in the function of T lymphocytes has never been previously investigated. Our present study was designed to determine whether β(1)-AA isolated from the sera of dilated cardiomyopathy (DCM) patients caused the proliferation of T cells and the secretion of cytokines.
methodsBlood samples were collected from 95 DCM patients as well as 95 healthy subjects, and β(1)-AA was detected using ELISA. The CD3(+)T lymphocytes were selected separately through flow cytometry and the effect of β(1)-AA on T lymphocyte proliferation was examined by CCK-8 kits and CFSE assay. Western blotting was used to analyze the expressions of phospho-VASP and phospho-p38 MAPK.
resultsβ(1)-AA enhanced the proliferation of T lymphocytes. This effect could be blocked by the selective β(1)-adrenergic receptor antagonist metoprolol, PKA inhibitor H89, and p38 MAPK inhibitor SB203580. Furthermore, the expression of the phosphorylated forms of phospho-VASP and phospho-p38 MAPK were markedly increased in the presence of β(1)-AA. β(1)-AA also inhibited the secretion of interferon-γ (IFN-γ) while promoting an increase in interleukin-4 (IL-4) levels.
conclusionsThese results demonstrate that β(1)-AA isolated from DCM patients binds to β(1)-AR on the surface of T cells, causing changes in T-cell proliferation and secretion through the β(1)-AR/cAMP/PKA and p38 MAPK pathways.
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