Evidence map›Paper›PMID 33968409›Full record

ReviewClinical & translational immunology2021

Autoantibodies against complement component C1q in systemic lupus erythematosus.

Marten Trendelenburg

Open access · goldAbstract readReview
In one paragraph

Review in Clinical & translational immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Article
  9. Reply.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Crystal structure ofFrontiers in immunology · 2024
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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 at 1 institution in 1 country.

Marten TrendelenburgDivision of Internal Medicine University Hospital Basel Basel Switzerland.ORCID https://orcid.org/0000-0001-7036-8386
University of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is the archetype of a systemic autoimmune disease, but the multifaceted pathogenic mechanisms leading to inflammation and organ damage are not fully understood. Homozygous deficiency of complement C1q, the first component of the classical pathway of complement, is strongly associated with the development of SLE, thus pointing at a primarily protective role of C1q. However, while most SLE patients do not have hereditary C1q deficiency, there is indirect evidence for the importance of C1q in the inflammatory processes of the disease, including hypocomplementemia as a result of activation via the classical pathway, deposition of C1q in affected tissues and the occurrence of autoantibodies against C1q (anti-C1q). The growing body of knowledge on anti-C1q led to the establishment of a biomarker that is used in the routine clinical care of SLE patients. Exploring the binding characteristics of anti-C1q allows to understand the mechanisms, that lead to the expression of relevant autoantigenic structures and the role of genetic as well as environmental factors. Lastly, the analysis of the pathophysiological consequences of anti-C1q is of importance because C1q, the target of anti-C1q, is a highly functional molecule whose downstream effects are altered by the binding of the autoantibody. This review summarises current study data on anti-C1q and their implications for the understanding of SLE.

Indexed as

anti‐C1q antibodiesC1qcomplementSLEsystemic lupus erythematosus

Identifiers

PMID33968409
PMCPMC8082710
OpenAlexW3158333192

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.