Evidence map›Paper›PMID 40710333›Full record

ReviewCells2025

Pathogenesis of Autoimmunity/Systemic Lupus Erythematosus (SLE).

Shunichi Shiozawa

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. 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

1 author.

Shunichi ShiozawaInstitute for Rheumatic Diseases, 60-14 Okuikeminamicho, Ashiya 659-0004, Japan.

Funding

Institute for Rheumatic Diseases, Ministry of Education, Culture, Sports, Science and Technology of Japan, and Japan Science and Technology Agency Grant-in-aid 25515003, 17659301, 13204059, 11557026, 12204074 and 0003 of Center of Excellence (CEO)
6 · The paper itself

Abstract

SLE is characterized by the generation of a variety of autoantibodies including anti-dsDNA autoantibodies, causing damage in various organs. If autoimmunity is defined by the generation of a variety of autoantibodies against the self, SLE is the only disease to qualify. Identification of the SLE-causing factor must fulfill the following criteria: (i) the factor induces SLE, (ii) the factor is operating in active SLE and (iii) SLE heals after removal of the factor. All candidate factors are reviewed from this viewpoint in this review. As to the cause of SLE, high levels of interferon α can induce SLE; however, interferon α in most patients did not reach this high level. BAFF (B cell activating factor of the TNF family) is increased in SLE. BAFF itself induced some manifestation of SLE, whereas removal of interferon α or BAFF by an antibody (Ab) did not heal SLE. BXSB male mice with a duplicated

Indexed as

AutoimmunityLupus Erythematosus, SystemicAnimalsAutoantibodiesB-Cell Activating FactorHumansMiceAutoantibodiesB-Cell Activating Factorautoimmunitypathogenesissystemic lupus erythematosus (SLE)T follicular helper cells (Tfh cells)

Identifiers

PMID40710333
PMCPMC12293469

What OpenQuestion holds

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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.