Evidence map›Paper›PMID 23749435›Full record

ArticleEuropean journal of immunology2013

Complement C4 maintains peripheral B-cell tolerance in a myeloid cell dependent manner.

Priyadarshini Chatterjee, Amma F Agyemang, Marat B Alimzhanov, Soren Degn, Stefanos A Tsiftsoglou, Elisabeth Alicot, Sarah A Jones, Minghe Ma, Michael C Carroll

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Dynamic control of autoreactive B cells from spontaneous germinal centers.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Immunogenetics of Lupus Erythematosus.Advances in experimental medicine and biology · 2022
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019
    Review
  17. Article
  18. Article
  19. 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

9 authors at 2 institutions in 1 country.

Priyadarshini Chatterjee *Program in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Amma F Agyemang *Program in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Marat B AlimzhanovProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Soren DegnProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Stefanos A TsiftsoglouProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Elisabeth AlicotProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Sarah A JonesProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Minghe MaProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Michael C CarrollProgram in Cellular and Molecular Medicine, Childrens Hospital, Harvard Medical School, Boston, MA, USA.
Cellular Research (United States) · USBoston Children's Hospital · US

Funding

Visualizing Effects of Costimulation on Antiviral ImmunityP01AI078897 · NIAID · HARVARD MEDICAL SCHOOL · PI VON ANDRIAN, ULRICH H · 2008 to 2012
$12.1M
COMPLEMENT SYSTEM AND HUMORAL IMMUNITYR01AI039246 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI CARROLL, MICHAEL CRAIG · 1996 to 2014
$6.1M
NIAID NIH HHS 1 P01 AI078897NIAID NIH HHS P01 AI078897NIAID NIH HHS R01 AI039246
6 · The paper itself

Abstract

The factors that allow self-reactive B cells to escape negative selection and become activated remain poorly defined. Using a BCR knock-in mouse strain, we identify a pathway by which B-cell selection to nucleolar self-antigens is complement dependent. Deficiency in complement component C4 led to a breakdown in the elimination of autoreactive B-cell clones at the transitional stage, characterized by a relative increase in their response to a range of stimuli, entrance into follicles, and a greater propensity to form self-reactive GCs. Using mixed BM chimeras, we found that the myeloid compartment was sufficient to restore negative selection in the autoreactive mice. A model is proposed in which in the absence of complement C4, inappropriate clearance of apoptotic debris promotes chronic activation of myeloid cells, allowing the maturation and activation of self-reactive B-cell clones leading to increased spontaneous formation of GCs.

Indexed as

Immune ToleranceAnimalsApoptosisAutoantigensAutoimmunityB-LymphocytesBone Marrow CellsComplement C4Lupus Erythematosus, SystemicLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMyeloid CellsNucleolus Organizer RegionReceptors, Antigen, B-CellAutoantigensC4b protein, mouseComplement C4Receptors, Antigen, B-CellRibonucleoproteinsAutoimmunityGerminal centerLupus nucleolar antigenNegative selection

Identifiers

PMID23749435
PMCPMC4086186
OpenAlexW1496216395

What OpenQuestion holds

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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.