Evidence map›Paper›PMID 25826676›Full record

ArticleMolecular medicine (Cambridge, Mass.)2015

Expression of Blimp-1 in dendritic cells modulates the innate inflammatory response in dextran sodium sulfate-induced colitis.

Sun Jung Kim, Jordan Goldstein, Kimberly Dorso, Miriam Merad, Lloyd Mayer, James M Crawford, Peter K Gregersen, Betty Diamond

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  13. Serum proteome of dogs with chronic enteropathy.Journal of veterinary internal medicine
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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 3 institutions in 1 country.

Sun Jung KimThe Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset, New York, United States of America.
Jordan GoldsteinThe Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset, New York, United States of America.
Kimberly DorsoThe Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset, New York, United States of America.
Miriam MeradThe Human Immunology Center, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Lloyd MayerThe Immunology Institute, Icahn School of Medicine at Mount Sinai (deceased), New York, New York, United States of America.
James M CrawfordDepartment of Pathology and Laboratory Medicine, Hofstra North Shore-LIJ School of Medicine, Hempstead, New York, United States of America.
Peter K GregersenDepartment of Molecular Medicine, School of Medicine, Hofstra University, Hempstead, New York, United States of America.
Betty DiamondThe Center for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Manhasset, New York, United States of America.
Feinstein Institute for Medical Research · USHofstra University · USIcahn School of Medicine at Mount Sinai · US

Funding

Function of Blimp1/prdm-1 in dendritic cells in the generation of autoantibodiesK01AR059378 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI KIM, SUN JUNG · 2010 to 2014
$568k
NIAMS NIH HHS K01 AR059378
6 · The paper itself

Abstract

A single nucleotide polymorphism of PRDM1, the gene encoding Blimp-1, is strongly associated with inflammatory bowel disease. Here, we demonstrate that Blimp-1 in CD103(+) dendritic cells (DCs) critically contributes to the regulation of macrophage homeostasis in the colon. Dextran sodium sulfate (DSS)-exposed Blimp-1(cko) mice with a deletion of Blimp-1 in CD103(+) DCs and CD11c(hi) macrophages exhibited severe inflammatory symptoms, pronounced weight loss, high mortality, robust infiltration of neutrophils in epithelial regions of the colon, an increased expression of proinflammatory cytokines and a significant decrease in CD103(+) DCs in the colon compared with DSS exposed wild-type (WT) mice. Purified colonic macrophages from Blimp-1(cko) mice expressed increased levels of matrix metalloproteinase 8, 9 and 12 mRNA. WT macrophages cocultured with colonic DCs but not bone marrow-derived DCs from Blimp-1(cko) produced increased matrix metalloproteinases in an interleukin (IL)-1β- and IL-6-dependent manner. Treatment of Blimp-1(cko) mice with anti-IL-1β and anti-IL-6 abrogated the exaggerated clinical response. Overall, these data demonstrate that Blimp-1 expression in DCs can alter an innate inflammatory response by modulating the activation of myeloid cells. This is a novel mechanism of contribution of Blimp-1 for the pathogenesis of inflammatory bowel diseases, implicating another therapeutic target for the development of inflammatory bowel disease.

Indexed as

AnimalsColitisCytokinesDendritic CellsDextran SulfateHumansMacrophagesMatrix MetalloproteinasesMice, Inbred BALB CMice, KnockoutPositive Regulatory Domain I-Binding Factor 1Repressor ProteinsTranscription FactorsCytokinesDextran SulfateMatrix MetalloproteinasesPositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanPrdm1 protein, mouseRepressor ProteinsTranscription Factors

Identifiers

PMID25826676
PMCPMC4398669
OpenAlexW2337084247

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.