Evidence map›Paper›PMID 24194774›Full record

ArticleClinical & developmental immunology2013

Altered sympathetic-to-immune cell signaling via β₂-adrenergic receptors in adjuvant arthritis.

Dianne Lorton, Denise L Bellinger, Jill A Schaller, Eric Shewmaker, Tracy Osredkar, Cheri Lubahn

Open access · goldAbstract read
In one paragraph

Article in Clinical & developmental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Driving βFrontiers in immunology · 2021
    Article
  3. Review
  4. Review
  5. βInflammopharmacology · 2019
    Article
  6. Review
  7. Norepinephrine Inhibits Th17 Cells via β2-Adrenergic Receptor (β2-AR) Signaling in a Mouse Model of Rheumatoid Arthritis.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  8. G protein coupled receptors signaling pathways implicate in inflammatory and immune response of rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Dianne LortonHoover Arthritis Research Center, Banner Health Research Institute, 10515 W. Santa Fe Drive, Sun City, AZ 85351, USA ; Department of Psychology, Kent State University, 133 Kent Hall, Kent, OH 44242, USA ; Kent-Summa Institute for Clinical and Translational Research, Summa Health System, 525 East Market Street, Akron,OH 44304, USA.
Denise L Bellinger
Jill A Schaller
Eric Shewmaker
Tracy Osredkar
Cheri Lubahn
Banner Health · USLoma Linda University · USSumma Health System · US

Funding

NINDS NIH HHS 1 R01 NS055673-01
6 · The paper itself

Abstract

Adjuvant-induced arthritic (AA) differentially affects norepinephrine concentrations in immune organs, and in vivo β-adrenergic receptor (β-AR) agonist treatment distinctly regulates ex vivo cytokine profiles in different immune organs. We examined the contribution of altered β-AR functioning in AA to understand these disparate findings. Twenty-one or 28 days after disease induction, we examined β₂-AR expression in spleen and draining lymph nodes (DLNs) for the arthritic limbs using radioligand binding and western blots and splenocyte β-AR-stimulated cAMP production using enzyme-linked immunoassay (EIA). During severe disease, β-AR agonists failed to induce splenocyte cAMP production, and β-AR affinity and density declined, indicating receptor desensitization and downregulation. Splenocyte β₂-AR phosphorylation (pβ₂-AR) by protein kinase A (pβ₂-AR(PKA)) decreased in severe disease, and pβ₂-AR by G protein-coupled receptor kinases (pβ₂-AR(GRK)) increased in chronic disease. Conversely, in DLN cells, pβ₂-AR(PKA) rose during severe disease, but fell during chronic disease, and pβ₂-AR(GRK) increased during both disease stages. A similar pβ₂-AR pattern in DLN cells with the mycobacterial cell wall component of complete Freund's adjuvant suggests that pattern recognition receptors (i.e., toll-like receptors) are important for DLN pβ₂-AR patterns. Collectively, our findings indicate lymphoid organ- and disease stage-specific sympathetic dysregulation, possibly explaining immune compartment-specific differences in β₂-AR-mediated regulation of cytokine production in AA and rheumatoid arthritis.

Indexed as

Signal TransductionAdrenergic beta-2 Receptor AgonistsAnimalsArthritis, ExperimentalCyclic AMPCyclic AMP-Dependent Protein KinasesGene ExpressionG-Protein-Coupled Receptor KinasesInterferon-gammaLymph NodesMalePhosphorylationProtein BindingRatsReceptors, Adrenergic, beta-2Severity of Illness IndexAdrenergic beta-2 Receptor AgonistsCyclic AMPCyclic AMP-Dependent Protein KinasesG-Protein-Coupled Receptor KinasesInterferon-gammaReceptors, Adrenergic, beta-2Terbutaline

Identifiers

PMID24194774
PMCPMC3806360
OpenAlexW2117620009

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.