Evidence map›Paper›PMID 37837660›Full record

ArticleInflammatory bowel diseases2024

Vedolizumab Efficacy Is Associated With Decreased Intracolonic Dendritic Cells, Not Memory T Cells.

Elisa K Boden, Ramya Kongala, Duncan C Hindmarch, Donna M Shows, Julius G Juarez, James D Lord

Open access · hybridAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2024. 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
4.4field-weighted citation impact, top 5% 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, 14 citations in OpenAlex.

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  5. When Checkpoint Inhibitors Break Barriers: Mechanisms and Challenges of irAEs of the Skin, Gastrointestinal Tract, and Lung.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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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

6 authors at 4 institutions in 1 country.

Elisa K BodenCenter for Translational Research, Benaroya Research Institute, Seattle, WA, USA.
Ramya KongalaCenter for Translational Research, Benaroya Research Institute, Seattle, WA, USA.
Duncan C HindmarchCenter for Translational Research, Benaroya Research Institute, Seattle, WA, USA.
Donna M ShowsCenter for Translational Research, Benaroya Research Institute, Seattle, WA, USA.
Julius G JuarezGI Drug Discovery, Takeda Pharmaceuticals, Cambridge, MA, USA.
James D LordCenter for Translational Research, Benaroya Research Institute, Seattle, WA, USA.ORCID 0000-0001-8961-3660
Benaroya Research InstituteOregon Health & Science University · USTakeda (United States) · USVirginia Mason Medical Center · US

Funding

Takeda Pharmaceuticals
6 · The paper itself

Abstract

backgroundVedolizumab, an antibody blocking integrin α4β7, is a safe and effective therapy for Crohn's disease and ulcerative colitis. Blocking α4β7 from binding its cognate addressin MAdCAM-1 on intestinal blood vessel endothelial cells prevents T cells from migrating to the gut mucosa in animal models. However, data supporting this mechanism of action in humans is limited.

methodsWe conducted a cross-sectional case-control study to evaluate the effect of vedolizumab on intestinal immune cell populations while avoiding the confounding effect of resolving inflammation on the cellularity of the colonic mucosa in treatment-responsive patients. Colon biopsies from 65 case subjects receiving vedolizumab were matched with biopsies from 65 control individuals, similar in disease type, medications, anatomic location, and inflammation. Biopsies were analyzed by flow cytometry and full messenger RNA transcriptome sequencing of sorted T cells.

resultsNo difference was seen between vedolizumab recipients and control individuals in the quantity of any antigen-experienced T lymphocyte subset or in the quality of the transcriptome in any experienced T cell subset. Fewer naïve colonic B and T cells were seen in vedolizumab recipients than control individuals, regardless of response. However, the most striking finding was a marked reduction in CD1c+ (BDCA1+) dendritic cells exclusively in vedolizumab-responsive patients. In blood, these dendritic cells ubiquitously express high levels of α4β7, which is rapidly downregulated upon vedolizumab exposure.

conclusionsThe clinical effects of vedolizumab reveal integrin α4β7-dependent dendritic cell migration to the intestinal mucosa to be central to inflammatory bowel disease pathogenesis.

Indexed as

Antibodies, Monoclonal, HumanizedDendritic CellsGastrointestinal AgentsIntestinal MucosaMemory T CellsAdultCase-Control StudiesColitis, UlcerativeColonCrohn DiseaseCross-Sectional StudiesFemaleHumansIntegrinsMaleMiddle AgedAntibodies, Monoclonal, HumanizedGastrointestinal Agentsintegrin alpha4beta7Integrinsvedolizumabdendritic cellintegrinT cellvedolizumab

Identifiers

PMID37837660
PMCPMC11063563
OpenAlexW4387638036

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.