Evidence map›Paper›PMID 29842945›Full record

ArticleClinical immunology (Orlando, Fla.)2018

Circulating integrin alpha4/beta7+ lymphocytes targeted by vedolizumab have a pro-inflammatory phenotype.

James D Lord, S Alice Long, Donna M Shows, Jerill Thorpe, Katherine Schwedhelm, Janice Chen, Mariko Kita, Jane H Buckner

Open access · hybridAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Update on Maintenance Immunosuppression in Intestinal Transplantation.Gastroenterology clinics of North America · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Mucosal integrin α4β7 blockade fails to reduce the seeding and size of viral reservoirs in SIV-infected rhesus macaques.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. 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

8 authors at 2 institutions in 2 countries.

James D LordBenaroya Research Institute, Translational Research Program, United States.. Electronic address: jlord@benaroyaresearch.org.
S Alice LongBenaroya Research Institute, Translational Research Program, United States.
Donna M ShowsBenaroya Research Institute, Translational Research Program, United States.
Jerill ThorpeBenaroya Research Institute, Translational Research Program, United States.
Katherine SchwedhelmBenaroya Research Institute, Translational Research Program, United States.
Janice ChenBenaroya Research Institute, Translational Research Program, United States.
Mariko KitaBenaroya Research Institute, Translational Research Program, United States.
Jane H BucknerBenaroya Research Institute, Translational Research Program, United States.
Translational Research Institute · AUBenchmark Research (United States) · US

Funding

Defining the role of altered cytokine signaling pathways on autoimmunityU01AI101990 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2016
$12.1M
NIAID NIH HHS U01 AI101990
6 · The paper itself

Abstract

Integrin alpha4/beta7 on circulating lymphocytes identifies them as gut-tropic, and can be targeted by the humanized antibody vedolizumab to treat inflammatory bowel disease (IBD). We found lymphocytes expressing alpha4/beta7 were significantly more responsive to the pro-inflammatory cytokines IL-6, IL-7, and IL-21, and less responsive to the regulatory T cell (Treg)-supporting cytokine IL-2. Alpha4/beta7 was expressed by a smaller percent of FOXP3 + Helios+ thymically-derived Tregs (tTregs) than FOXP3 + Helios- peripherally-derived Tregs (pTregs) or FOXP3- effector T cells. Integrin alpha4/beta7+ CD4 T cells were also rare among cells expressing the Th2 marker CRTh2, but enriched in cells bearing the circulating T follicular helper cell marker CXCR5. Thus the effect of this anti-integrin therapy on the mucosal immune system may be more qualitative than quantitative, and selectively replace pro-inflammatory effector cells with Tregs and Th2 cells to facilitate immune tolerance in the mucosa without globally depleting lymphocytes from the intestinal mucosa.

Indexed as

AdultAntibodies, Monoclonal, HumanizedBlood CirculationCytokinesFemaleForkhead Transcription FactorsGastrointestinal AgentsHumansIkaros Transcription FactorImmune ToleranceInflammation MediatorsInflammatory Bowel DiseasesIntegrinsIntestinesMaleMiddle AgedAntibodies, Monoclonal, HumanizedCXCR5 protein, humanCytokinesForkhead Transcription FactorsFOXP3 protein, humanGastrointestinal AgentsIkaros Transcription FactorIKZF2 protein, humanInflammation Mediatorsintegrin alpha4beta7IntegrinsReceptors, CXCR5vedolizumabCrohn's diseasecT(FH)FOXP3HeliosIL-2, IL-6, IL-7, IL-21IntegrinStatTh1Th2TregVedolizumab

Identifiers

PMID29842945
PMCPMC6257989
OpenAlexW2804487242

What OpenQuestion holds

Textmetadata
LicenceTDM
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.