Evidence map›Paper›PMID 34817551›Full record

ArticleThe Journal of experimental medicine2021

DCIR and its ligand asialo-biantennary N-glycan regulate DC function and osteoclastogenesis.

Tomonori Kaifu, Rikio Yabe, Takumi Maruhashi, Soo-Hyun Chung, Hiroaki Tateno, Noriyuki Fujikado, Jun Hirabayashi, Yoichiro Iwakura

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. The C-type lectin receptor Dcir (Frontiers in immunology · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Regulation of Glycosylation in Bone Metabolism.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. From structure to function - Ligand recognition by myeloid C-type lectin receptors.Computational and structural biotechnology journal · 2022
    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

8 authors at 2 institutions in 1 country.

Tomonori Kaifu *Center for Animal Disease Models, Research Institution for Biological Sciences, Tokyo University of Science, Yamazaki, Noda, Chiba, Japan.ORCID 0000-0002-2614-1472
Rikio Yabe *Center for Animal Disease Models, Research Institution for Biological Sciences, Tokyo University of Science, Yamazaki, Noda, Chiba, Japan.ORCID 0000-0001-7542-8819
Takumi Maruhashi *Center for Animal Disease Models, Research Institution for Biological Sciences, Tokyo University of Science, Yamazaki, Noda, Chiba, Japan.ORCID 0000-0003-2944-1611
Soo-Hyun Chung *Center for Animal Disease Models, Research Institution for Biological Sciences, Tokyo University of Science, Yamazaki, Noda, Chiba, Japan.ORCID 0000-0003-2808-1327
Hiroaki TatenoGlycan Lectin Engineering Team, Research Center for Stem Cell Engineering, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan.ORCID 0000-0003-3006-1659
Noriyuki FujikadoCenter for Animal Disease Models, Research Institution for Biological Sciences, Tokyo University of Science, Yamazaki, Noda, Chiba, Japan.ORCID 0000-0002-0415-5929
Jun HirabayashiGlycan Lectin Engineering Team, Research Center for Stem Cell Engineering, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan.ORCID 0000-0002-8571-359X
Yoichiro IwakuraCenter for Animal Disease Models, Research Institution for Biological Sciences, Tokyo University of Science, Yamazaki, Noda, Chiba, Japan.ORCID 0000-0002-9934-5775
Tokyo University of Science · JPNational Institute of Advanced Industrial Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cell immunoreceptor (DCIR) is a C-type lectin receptor with a carbohydrate recognition domain and an immunoreceptor tyrosine-based inhibitory motif. Previously, we showed that Dcir-/- mice spontaneously develop autoimmune enthesitis and sialadenitis, and also develop metabolic bone abnormalities. However, the ligands for DCIR functionality remain to be elucidated. Here we showed that DCIR is expressed on osteoclasts and DCs and binds to an asialo-biantennary N-glycan(s) (NA2) on bone cells and myeloid cells. Osteoclastogenesis was enhanced in Dcir-/- cells, and NA2 inhibited osteoclastogenesis. Neuraminidase treatment, which exposes excess NA2 by removing the terminal sialic acid of N-glycans, suppressed osteoclastogenesis and DC function. Neuraminidase treatment of mice ameliorated collagen-induced arthritis and experimental autoimmune encephalomyelitis in a DCIR-dependent manner, due to suppression of antigen presentation by DCs. These results suggest that DCIR activity is regulated by the modification of the terminal sialylation of biantennary N-glycans, and this interaction is important for the control of both autoimmune and bone metabolic diseases.

Indexed as

AnimalsArthritis, ExperimentalCells, CulturedDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalHEK293 CellsHumansLectins, C-TypeMembrane GlycoproteinsMiceMice, Inbred C57BLMice, Mutant StrainsMice, TransgenicN-AcetylglucosaminyltransferasesNeuraminidaseOsteoclastsalpha-1,6-mannosyl-glycoprotein beta-1,2-N-acetylglucosaminyltransferaseCLEC4A protein, humanDcir protein, mouseLectins, C-TypeMembrane GlycoproteinsN-AcetylglucosaminyltransferasesNeuraminidasePolysaccharidesReceptors, Immunologic

Identifiers

PMID34817551
PMCPMC8624811
OpenAlexW3216358361

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.