Cited by 48Systemic Lupus Erythematosus ResearchComplement system in diseasesVasculitis and related conditions

Autoantibodies against complement component C1q in systemic lupus erythematosus

Open access
Trendelenburg, Marten·2021·Clinical & Translational Immunology

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1002/cti2.1279

Cites

101 of 101 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. [48]Siegert CE, Daha MR, Halma C, van der Voort EA, Breedveld FC. IgG and IgA autoantibodies to C1q in systemic and renal diseases. Clin Exp Rheumatol 1992; 10: 19– 23. 1348021

Cited by

Sorted by citations

Authors
Trendelenburg, M.
Affiliations
University of Basel (CH)
Corresponding author
Trendelenburg, Marten
Venue
Clinical & Translational Immunology
Publisher
Wiley
Published
2021-01
Volume
10
Issue
4
Pages
e1279-e1279
ISSN
2050-0068 (ISSN-L)
OpenAlex
W3158333192
Cited by
48
References
101
Citations by year
2026: 7 · 2025: 7 · 2024: 15 · 2023: 5 · 2022: 10 · 2021: 3
FWCI
1.35
Type
journal article
Language
en
Open access
Locations
  • Clinical & Translational Immunology (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Science Foundation
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (172965, 310030)
  • Idorsia Pharmaceuticals
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Vasculitis and related conditions
Keywords
systemic lupus erythematosus, C1q, anti-C1q autoantibodies, C1q deficiency, classical complement pathway, hypocomplementemia, autoantigens, biomarkers, lupus pathogenesis

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review