Evidence map›Paper›PMID 23238564›Full record

ArticleCell death and differentiation2013

SIGN-R1, a C-type lectin, enhances apoptotic cell clearance through the complement deposition pathway by interacting with C1q in the spleen.

M G Prabagar, Y Do, S Ryu, J-Y Park, H-J Choi, W-S Choi, T J Yun, J Moon, I-S Choi, K Ko and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. C1q as a potential tolerogenic therapeutic in transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. C1q: A fresh look upon an old molecule.Molecular immunology · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Complement Protein C1q Interacts with DC-SIGNFrontiers in immunology · 2016
    Article
  16. Review
  17. Article
  18. Bacterial Infections Following Splenectomy for Malignant and Nonmalignant Hematologic Diseases.Mediterranean journal of hematology and infectious diseases · 2015
    Review
  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

14 authors at 6 institutions in 3 countries.

M G PrabagarDepartment of Biomedical Science and Technology, SMART Institute of Advanced Biomedical Science, Institute of Functional Genomics, Konkuk University, 1 Hwayang-dong, Gwangjin-gu, Seoul 143-701, Republic of Korea.
Y Do
S Ryu
J-Y Park
H-J Choi
W-S Choi
T J Yun
J Moon
I-S Choi
K Ko
K Ko
C Young Shin
C Cheong
Y-S Kang
Konkuk University · KRUniversité de Montréal · CACornell University · USDaegu-Gyeongbuk Medical Innovation Foundation · KRMontreal Clinical Research Institute · CAUlsan National Institute of Science and Technology · KR

Funding

Improved plague vaccine by targeting dendritic cell subsetsR21AI082331 · NIAID · ROCKEFELLER UNIVERSITY · PI DO, YOONKYUNG · 2009 to 2010
$465k
NIAID NIH HHS 1R21AI082331-01NIAID NIH HHS R21 AI082331
6 · The paper itself

Abstract

Complements, such as C1q and C3, and macrophages in the splenic marginal zone (MZMs) play pivotal roles in the efficient uptake and processing of circulating apoptotic cells. SIGN-R1, a C-type lectin that is highly expressed in a subpopulation of MZMs, regulates the complement fixation pathway by interacting with C1q, to fight blood-borne Streptococcus pneumoniae. Therefore, we examined whether the SIGN-R1-mediated classical complement pathway plays a role in apoptotic cell clearance and immune tolerance. SIGN-R1 first-bound apoptotic cells and this binding was significantly enhanced in the presence of C1q. SIGN-R1-C1q complex then immediately mediated C3 deposition on circulating apoptotic cells in the MZ, leading to the efficient clearance of them. SIGN-R1-mediated C3 deposition was completely abolished in the spleen of SIGN-R1 knockout (KO) mice. Given that SIGN-R1 is not expressed in the liver, we were struck by the finding that C3-deposited apoptotic cells were still found in the liver of wild-type mice, and dramatically reduced in the SIGN-R1 KO liver. In particular, SIGN-R1 deficiency caused delayed clearance of apoptotic cells and aberrant secretion of cytokines, such as TNF-α, IL-6, and TGF-β in the spleen as well as in the liver. In addition, anti-double- and single-stranded DNA antibody level was significantly increased in SIGN-R1-depleted mice compared with control mice. These findings suggest a novel mechanism of apoptotic cell clearance which is initiated by SIGN-R1 in the MZ and identify an integrated role of SIGN-R1 in the systemic clearance of apoptotic cells, linking the recognition of apoptotic cells, the opsonization of complements, and the induction of immune tolerance.

Indexed as

AnimalsApoptosisCell Adhesion MoleculesCells, CulturedCHO CellsComplement C1qComplement C3CricetinaeCricetulusDC-Specific ICAM-3 Grabbing NonintegrinDNA, Single-StrandedHumansInterleukin-10Interleukin-6Jurkat CellsLectins, C-TypeCell Adhesion MoleculesComplement C1qComplement C3DC-Specific ICAM-3 Grabbing NonintegrinDNA, Single-StrandedInterleukin-10Interleukin-6Lectins, C-TypeReceptors, Cell SurfaceRNA, Small InterferingTransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID23238564
PMCPMC3595488
OpenAlexW2054533099

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.