Evidence map›Paper›PMID 25854151›Full record

ArticleZeitschrift fur Rheumatologie2015

[Pathogenesis of systemic lupus erythematosus].

T Alexander, A Radbruch, F Hiepe

Abstract readEnglish Abstract
PubMed Publisher
In one paragraph

Article in Zeitschrift fur Rheumatologie, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. [Immunopathogenesis of systemic lupus erythematosus].Zeitschrift fur Rheumatologie · 2024
    Review
  2. 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

3 authors.

T AlexanderMedizinische Klinik m. S. Rheumatologie und Klinische Immunologie, Charité - Universitätsmedizin Berlin; Deutsches RheumaForschungszentrum Berlin - ein Institut der Leibniz-Gemeinschaft, Charitéplatz 1, 10117, Berlin, Deutschland.
A Radbruch
F Hiepe

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease with an extremely complex pathogenesis. Due to a genetic predisposition the disease can be induced by multiple stress factors involving epigenetic mechanisms and under the influence of the innate immune system. Defective clearance of immune complexes and apoptotic material together with enhanced neutrophil extracellular trap formation (NETosis) as well as up-regulation of type 1 interferon in particular, drive the adaptive immune system to a breakdown of self-tolerance. The result is a B cell hyperactivity, which leads to the generation of a multitude of different autoantibodies that are not only directed against nuclear antigens. Autoantibodies are the initiators for the involvement of many organs, which enhances further inflammatory cells and cytokines by participation of effector T-cells. Finally, an autoreactive immunological (plasma cell) memory is formed, which contributes to chronification and is associated with therapy-refractive courses of the disease. The depletion of the autoreactive immunological memory by immunoablation can lead to induction of self-tolerance and long-term remission.

Indexed as

AutoantibodiesCytokinesGenetic Predisposition to DiseaseHumansImmunity, InnateLupus Erythematosus, SystemicModels, GeneticModels, ImmunologicalAutoantibodiesCytokines

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.