Evidence map›Paper›PMID 31044336›Full record

SynthesisJournal of clinical immunology2019

Ficolin-3 Deficiency Is Associated with Disease and an Increased Risk of Systemic Lupus Erythematosus.

Anne Troldborg, Rudi Steffensen, Marten Trendelenburg, Thomas Hauser, Kasper G Winther, Annette G Hansen, Kristian Stengaard-Pedersen, Anne Voss, Steffen Thiel

Abstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Journal of clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
    Article
  4. The Complement System.Advances in experimental medicine and biology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Deimination Protein Profiles inFrontiers in immunology · 2020
    Article
  15. Article
  16. Article
  17. 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

9 authors at 5 institutions in 2 countries.

Anne TroldborgDepartment of Rheumatology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark. annetrol@rm.dk.ORCID 0000-0002-9501-1268
Rudi SteffensenDepartment of Clinical Immunology, Aalborg University Hospital, Aalborg, Denmark.
Marten TrendelenburgDivision of Internal Medicine and Clinical Immunology lab, Department of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.
Thomas HauserIZZ Immunologie-Zentrum Zürich, Zürich, Switzerland.
Kasper G WintherDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Annette G HansenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Kristian Stengaard-PedersenDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Anne VossDepartment of Rheumatology, Odense University Hospital, Odense, Denmark.
Steffen ThielDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Aarhus University · DKAalborg University Hospital · DKImmunologie-Zentrum Zürich · CHOdense University Hospital · DKUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeFicolin-3 deficiency is caused by a mutation (+1637delC) in the FCN3 gene. It is a rare condition and has been associated with both infection and autoimmune disease including systemic lupus erythematosus (SLE). Here we investigated if ficolin-3 deficiency is more frequent in patients than in controls and tried to identify a common phenotype among ficolin-3 deficient individuals. Since a significant part of patients identified with ficolin-3 deficiency was diagnosed with SLE, we explored whether the heterozygous state of the FCN3+1637delC variant represents a risk factor in the development of SLE. Further, we examined other possible causes of ficolin-3 deficiency when the FCN3+1637delC is not present.

methodsA systematic literature search for studies measuring ficolin-3 was carried out. We examined 362 SLE patients and 596 controls for the presence of the variant FCN3+1637delC. We established assays for measurements of ficolin-3 and of auto-antibodies against ficolin-3. We sequenced the coding and non-coding regions of the FCN3 gene in an SLE patient with ficolin-3 deficiency not carrying the +1637delC.

resultsFicolin-3 deficiency leads to an 8-time increased odds of having a disease (p < 0.05). Three out of nine patients with deficiency had SLE. The heterozygous state of the deficiency variant is not associated with increased risk of developing SLE (p = 0.18).

conclusionBy systematically reviewing the literature for the described cases of ficolin-3 deficiency, an autoimmune phenotype is emerging. Thirty-three percent of the ficolin-3 deficient patients had SLE. Heterozygosity for the FCN3 gene deletion causing the deficiency does not seem to be associated with the development of SLE.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseAllelesFemaleGenetic TestingGenotypeHumansLectinsLupus Erythematosus, SystemicMaleMutationPhenotypeRisk AssessmentSequence Analysis, DNAFCN3 protein, humanLectinsautoimmunitycomplementcomplement deficiencyficolin-3 deficiencySLE

Identifiers

PMID31044336
OpenAlexW2943511292

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.