Evidence map›Paper›PMID 26376366›Full record

ArticleMucosal immunology2016

CD4 T cells are required for both development and maintenance of disease in a new mouse model of reversible colitis.

J Brasseit, E Althaus-Steiner, M Faderl, N Dickgreber, L Saurer, V Genitsch, T Dolowschiak, H Li, D Finke, W-D Hardt and 5 more

Abstract read
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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 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.5field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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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

15 authors at 3 institutions in 1 country.

J BrasseitDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
E Althaus-SteinerDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
M FaderlDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
N DickgreberDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
L SaurerDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
V GenitschDivision of Clinical Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
T DolowschiakInstitute of Microbiology, ETH Zürich, Zurich, Switzerland.
H LiMaurice E. Müller Laboratories, University Clinic for Visceral Surgery and Medicine, University of Bern, Bern, Switzerland.
D FinkeDivision of Developmental Immunology, Department of Biomedicine, University of Basel, Basel, Switzerland.
W-D HardtInstitute of Microbiology, ETH Zürich, Zurich, Switzerland.
K D McCoyMaurice E. Müller Laboratories, University Clinic for Visceral Surgery and Medicine, University of Bern, Bern, Switzerland.
A J MacphersonMaurice E. Müller Laboratories, University Clinic for Visceral Surgery and Medicine, University of Bern, Bern, Switzerland.
N CorazzaDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
M NotiDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
C MuellerDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
University of Bern · CHETH Zurich · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current therapies to treat inflammatory bowel diseases have limited efficacy, significant side effects, and often wane over time. Little is known about the cellular and molecular mechanisms operative in the process of mucosal healing from colitis. To study such events, we developed a new model of reversible colitis in which adoptive transfer of CD4(+)CD45RB(hi) T cells into Helicobacter typhlonius-colonized lymphopenic mice resulted in a rapid onset of colonic inflammation that was reversible through depletion of colitogenic T cells. Remission was associated with an improved clinical and histopathological score, reduced immune cell infiltration to the intestinal mucosa, altered intestinal gene expression profiles, regeneration of the colonic mucus layer, and the restoration of epithelial barrier integrity. Notably, colitogenic T cells were not only critical for induction of colitis but also for maintenance of disease. Depletion of colitogenic T cells resulted in a rapid drop in tumor necrosis factor α (TNFα) levels associated with reduced infiltration of inflammatory immune cells to sites of inflammation. Although neutralization of TNFα prevented the onset of colitis, anti-TNFα treatment of mice with established disease failed to resolve colonic inflammation. Collectively, this new model of reversible colitis provides an important research tool to study the dynamics of mucosal healing in chronic intestinal remitting-relapsing disorders.

Indexed as

Adoptive TransferAnimalsCD4-Positive T-LymphocytesCell MovementCells, CulturedColitisDisease Models, AnimalGene Expression RegulationHelicobacter InfectionsHumansInflammatory Bowel DiseasesIntestinal MucosaLymphocyte DepletionMiceMice, Inbred C57BLMice, KnockoutTumor Necrosis Factor-alpha

Identifiers

PMID26376366
OpenAlexW2313524676

What OpenQuestion holds

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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.