Evidence map›Paper›PMID 18213527›Full record

ReviewImmunologic research2008

B-cell involvement in the pathogenesis of RA-is there a contribution of the sympathetic nervous system?

Georg Pongratz, Rainer H Straub

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Rheumatoid arthritis: Disease or syndrome?Open access rheumatology : research and reviews · 2009
    Review
  3. Review
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

2 authors.

Georg PongratzDepartment of Internal Medicine I, Laboratory of Neuroendocrinoimmunology, University Hospital Regensburg, Regensburg 93042, Germany.
Rainer H Straub

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of rheumatoid arthritis (RA), the most common rheumatic disease, is still an unsolved puzzle. For many years, T-cells were the main focus of research, but recently, the B-cell drew more and more attention not least, due to the observation in humans that the anti-CD20 antibody Retuximab, which selectively depletes subsets of B-cells, lessens disease symptoms. A second novel approach to understand pathomechanisms that contribute to the development and progression of arthritis focuses on the sympathetic nervous system, which is known to moderate the function of immune cells, e.g., the B-cell, and therefore, is tied into a complex neuroimmune network that influences the course of the disease. This review first discusses current research that shows the significance of B-cells in the pathogenesis of RA. It then gives a short review of knowledge regarding the role of the sympathetic nervous system (1) in RA pathogenesis and (2) in modulating B-cell responses. Finally, the hypothesis is introduced that the sympathetic nervous system via modulating B-cell function, e.g., antibody production, influences the development and progression of RA.

Indexed as

AutoantibodiesAntibodies, MonoclonalAntibodies, Monoclonal, Murine-DerivedAntibody FormationAntigen PresentationAntigens, CD20Arthritis, RheumatoidAutoimmunityB-LymphocytesCytokinesHumansLymphocyte ActivationRituximabSympathetic Nervous SystemAntibodies, MonoclonalAntibodies, Monoclonal, Murine-DerivedAntigens, CD20AutoantibodiesCytokinesRituximab

Identifiers

What OpenQuestion holds

Textmetadata
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.