Evidence map›Paper›PMID 25204675›Full record

ArticleMucosal immunology2015

Dendritic cell CD83 homotypic interactions regulate inflammation and promote mucosal homeostasis.

J M Bates, K Flanagan, L Mo, N Ota, J Ding, S Ho, S Liu, M Roose-Girma, S Warming, L Diehl

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
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  15. Article
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  17. Article
  18. NR4A Expression by Human Marginal Zone B-Cells.Antibodies (Basel, Switzerland) · 2019
    Article
  19. Review
  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

10 authors at 1 institution.

J M BatesDepartment of Pathology, Genetech, South San Francisco, California, USA.
K FlanaganDepartment of Pathology, Genetech, South San Francisco, California, USA.
L MoDepartment of Pathology, Genetech, South San Francisco, California, USA.
N OtaDepartment of Immunology, Genetech, South San Francisco, California, USA.
J DingDepartment of Immunology, Genetech, South San Francisco, California, USA.
S HoDepartment of Pathology, Genetech, South San Francisco, California, USA.
S LiuDepartment of Pathology, Genetech, South San Francisco, California, USA.
M Roose-GirmaDepartment of Molecular Biology, Genentech, South San Francisco, California, USA.
S WarmingDepartment of Molecular Biology, Genentech, South San Francisco, California, USA.
L DiehlDepartment of Pathology, Genetech, South San Francisco, California, USA.
Genentech

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells (DCs) form an extensive network in the intestinal lamina propria, which orchestrates the mucosal immune response. Alterations in DC function can predispose to inflammatory bowel disease, although by unknown mechanisms. We show that CD83, a highly regulated DC cell surface protein, modulates the immune response to prevent colitis. Mice with a conditional knockout of CD83 in DCs develop exacerbated colitis following dextran sodium sulfate challenge, whereas mucosal overexpression of CD83 inhibits DC inflammatory response and protects against colitis. These CD83 perturbations can be modeled in vitro where we show that CD83 homotypic interaction occurs via cell-cell contact and inhibits pro-inflammatory responses. CD83 knockdown or cytoplasmic truncation abrogates the effects of homotypic binding. We demonstrate that CD83 homotypic interaction regulates DC activation via the mitogen-activated protein kinase pathway by inhibiting p38α phosphorylation. Our findings indicate that CD83 homotypic interactions regulate DC activation and promote mucosal homeostasis.

Indexed as

HomeostasisAnimalsAntigens, CDAntigens, SurfaceCD83 AntigenCell CommunicationColitisDendritic CellsDisease Models, AnimalFemaleGene ExpressionImmunity, MucosalImmunoglobulinsImmunophenotypingInflammationIntestinal MucosaAntigens, CDAntigens, SurfaceCD83 AntigenImmunoglobulinsMembrane Glycoproteins

Identifiers

PMID25204675
PMCPMC4326976
OpenAlexW1996686270

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.