Evidence map›Paper›PMID 26174764›Full record

ArticleMucosal immunology2016

Intestinal CD103(+)CD11b(-) dendritic cells restrain colitis via IFN-γ-induced anti-inflammatory response in epithelial cells.

A R B M Muzaki, P Tetlak, J Sheng, S C Loh, Y A Setiagani, M Poidinger, F Zolezzi, K Karjalainen, C Ruedl

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 126 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Regional and Sex-Dependent Immune Profiling Across the Colon in A Mouse Model of Ulcerative Colitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Type 1 and CD103European journal of immunology · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Synergistic Modulation of the Gut-Brain-Immune Axis by a DualJournal of microbiology and biotechnology · 2025
    Article
  11. Review
  12. ProbioticAntioxidants (Basel, Switzerland) · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023
    Article
  20. Article

26 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

A R B M MuzakiSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
P TetlakSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
J ShengSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
S C LohSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Y A SetiaganiSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
M PoidingerSingapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore.
F ZolezziSingapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore.
K KarjalainenSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
C RuedlSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Nanyang Technological University · SGAgency for Science, Technology and Research · SGSingapore Immunology Network · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A crosstalk between commensals, gut immune cells, and colonic epithelia is required for a proper function of intestinal mucosal barrier. Here we investigated the importance of two distinct intestinal dendritic cell (DC) subsets in controlling intestinal inflammation. We show that Clec9A-diphtheria toxin receptor (DTR) mice after depletion of CD103(+)CD11b(-) DCs developed severe, low-dose dextran sodium sulfate (DSS)-induced colitis, whereas the lack of CD103(+)CD11b(+) DCs in Clec4a4-DTR mice did not exacerbate intestinal inflammation. The CD103(+)CD11b(-) DC subset has gained a functional specialization that able them to repress inflammation via several epithelial interferon-γ (IFN-γ)-induced proteins. Among others, we identified that epithelial IDO1 and interleukin-18-binding protein (IL-18bp) were strongly modulated by CD103(+)CD11b(-) DCs. Through its preferential property to express IL-12 and IL-15, this particular DC subset can induce lymphocytes in colonic lamina propria and in epithelia to secrete IFN-γ that then can trigger a reversible early anti-inflammatory response in intestinal epithelial cells.

Indexed as

AnimalsAntigens, CDCD11b AntigenColitisColonDendritic CellsDextran SulfateDisease ResistanceEpithelial CellsFemaleGene Expression RegulationHeparin-binding EGF-like Growth FactorIndoleamine-Pyrrole 2,3,-DioxygenaseIntegrin alpha ChainsIntercellular Signaling Peptides and ProteinsInterferon-gammaalpha E integrinsAntigens, CDCD11b AntigenClec9a protein, mouseDextran SulfateHeparin-binding EGF-like Growth FactorIDO1 protein, mouseIndoleamine-Pyrrole 2,3,-DioxygenaseIntegrin alpha ChainsIntercellular Signaling Peptides and ProteinsInterferon-gammaInterleukin-12Interleukin-15interleukin-18 binding proteinLectins, C-TypeReceptors, Immunologic

Identifiers

PMID26174764
PMCPMC4801902
OpenAlexW2319211023

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.