Evidence map›Paper›PMID 29910804›Full record

ArticleFrontiers in immunology2018

Targeting Inflammatory T Helper Cells

Vera Buchele, Benjamin Abendroth, Maike Büttner-Herold, Tina Vogler, Johanna Rothamer, Sakhila Ghimire, Evelyn Ullrich, Ernst Holler, Markus F Neurath, Kai Hildner

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Novel T cell/organoid culture system allowsFrontiers in immunology · 2023
    Article
  3. Article
  4. Review
  5. Review
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 3 institutions in 1 country.

Vera BucheleDepartment of Medicine 1, University Hospital Erlangen, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.
Benjamin AbendrothDepartment of Medicine 1, University Hospital Erlangen, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.
Maike Büttner-HeroldDepartment of Nephropathology, Institute of Pathology, University Hospital Erlangen, Erlangen, Germany.
Tina VoglerDepartment of Medicine 1, University Hospital Erlangen, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.
Johanna RothamerDepartment of Medicine 5, University Hospital Erlangen, University of Erlangen-Nuremberg, Erlangen, Germany.
Sakhila GhimireDepartment of Hematology and Oncology, Regensburg University Hospital, Regensburg, Germany.
Evelyn UllrichDepartment of Medicine 5, University Hospital Erlangen, University of Erlangen-Nuremberg, Erlangen, Germany.
Ernst HollerDepartment of Hematology and Oncology, Regensburg University Hospital, Regensburg, Germany.
Markus F NeurathDepartment of Medicine 1, University Hospital Erlangen, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.
Kai HildnerDepartment of Medicine 1, University Hospital Erlangen, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.
Universitätsklinikum Erlangen · DEUniversity Hospital Regensburg · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal graft-versus-host disease (GvHD) is a life-threatening, inflammatory donor T cell-mediated complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT). In the light of the reported efficacy of interleukin-23 (IL-23)-blockade to mitigate syngeneic intestinal inflammation in inflammatory bowel disease patients, targeting IL-23 and thereby interleukin-17a (IL-17a) producing T helper (Th17) cells as the T cell subset assumed to be mostly regulated by IL-23, has emerged as a putatively general concept to harness immune-mediated mucosal inflammation irrespective of the underlying trigger. However, the role of Th17 cells during allo-response driven colitis remains ambiguous due to a series of studies with inconclusive results. Interestingly, we recently identified granulocyte-macrophage colony-stimulating factor (GM-CSF

Indexed as

AnimalsBone Marrow TransplantationCells, CulturedColitisDisease Models, AnimalFemaleGraft vs Host DiseaseMiceNuclear Receptor Subfamily 1, Group F, Member 3Receptors, InterleukinReceptors, Retinoic AcidRetinoic Acid Receptor gammaT-Lymphocytes, Helper-InducerT-Lymphocyte SubsetsTransplantation, Homologousinterleukin-23 receptor, mouseNuclear Receptor Subfamily 1, Group F, Member 3Receptors, InterleukinReceptors, Retinoic AcidRetinoic Acid Receptor gammabasic leucine zipper transcription factor ATF-likecolitisgranulocyte-macrophage colony-stimulating factorinterleukin-23 receptorintestinal graft-versus-host diseaseretinoic acid-related orphan receptor gamma tT helper 17 cells

Identifiers

PMID29910804
PMCPMC5992389
OpenAlexW2802388795

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.