Evidence map›Paper›PMID 25860947›Full record

ReviewInternational journal of molecular sciences2015

Pathogenesis of renal disease in systemic lupus erythematosus--the role of autoantibodies and lymphocytes subset abnormalities.

Desmond Y H Yap, Kar N Lai

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Review
  6. Article
  7. Article
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  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. AlteredDiagnostics (Basel, Switzerland) · 2022
    Article
  16. B Cell Aberrance in Lupus: the Ringleader and the Solution.Clinical reviews in allergy & immunology · 2022
    Review
  17. Article
  18. Article
  19. Rapamycin relieves lupus nephritis by regulating TIM-3 and CD4Central-European journal of immunology · 2022
    Article
  20. 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

2 authors at 2 institutions in 2 countries.

Desmond Y H YapNephrology Division, Department of Medicine, The University of Hong Kong, Hong Kong, China. drdesmondyap@gmail.com.
Kar N LaiNephrology Division, Department of Medicine, The University of Hong Kong, Hong Kong, China. knlai@hku.hk.
Chinese University of Hong Kong · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lupus nephritis (LN) is a common and severe organ manifestation of systemic lupus erythematosus (SLE), and is associated with significant patient morbidity and mortality. Autoantibodies and aberrations in lymphocyte subsets have putative roles in the pathogenesis of SLE and LN, and might reflect disease activity and are amenable to immunosuppressive treatments. Anti-DNA is one of the well-studied autoantibodies, which correlates with disease activity and has direct nephritogenic effects on resident renal cells and various glomerular components. Other important autoantibodies in the pathogenesis of LN include anti-C1q, anti-α-actinin and anti-nucleosome antibodies. Changes in naive and memory B cells and plasma cells have been observed in SLE and LN patients. These B cell subsets exert diverse effects during pathogenesis of LN such as production of autoantibodies, secretion of proinflammatory and anti-inflammatory cytokines and presentation of auto-antigens to effector cells. Aberration of T lymphocytes, especially the T-helper subsets, is also highly pertinent in the development of LN. In this context, important T helper subsets include Th1, Th2, Th9, Th17, TReg and follicular T-helper cells. The growing knowledge on these autoantibodies and lymphocyte subset abnormalities will enhance our understanding of SLE and LN, and hence help devise better strategies for disease monitoring and treatment.

Indexed as

AutoantibodiesB-LymphocytesHumansKidney DiseasesLupus Erythematosus, SystemicLupus NephritisT-Lymphocytes, Helper-InducerAutoantibodies

Identifiers

PMID25860947
PMCPMC4425058
OpenAlexW2023138787

What OpenQuestion holds

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LicenceCC BY
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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.