Evidence map›Paper›PMID 21093318›Full record

ArticleImmunity2010

Regulated expression of nuclear receptor RORγt confers distinct functional fates to NK cell receptor-expressing RORγt(+) innate lymphocytes.

Cedric Vonarbourg, Arthur Mortha, Viet L Bui, Pedro P Hernandez, Elina A Kiss, Thomas Hoyler, Melanie Flach, Bertram Bengsch, Robert Thimme, Christoph Hölscher and 6 more

Abstract read
In one paragraph

Article in Immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 411 papers.

0numbers the graph read from it
0cells of the map it votes in
411citing papers in PubMed
13.2field-weighted citation impact, top 1% 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

411 citing papers in PubMed, 648 citations in OpenAlex.

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351 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 10 institutions in 3 countries.

Cedric VonarbourgIMMH, Institute of Medical Microbiology & Hygiene, University of Freiburg, 79104 Freiburg, Germany. cedric.vonarbourg@uniklinik-freiburg.de
Arthur Mortha
Viet L Bui
Pedro P Hernandez
Elina A Kiss
Thomas Hoyler
Melanie Flach
Bertram Bengsch
Robert Thimme
Christoph Hölscher
Manfred Hönig
Ulrich Pannicke
Klaus Schwarz
Carl F Ware
Daniela Finke
Andreas Diefenbach
University of Freiburg · DECluster of Excellence "Inflammation at Interfaces"Immungenetics (Germany) · DEInstitute of Medical Microbiology and Hygiene · DEMax Planck Institute of Immunobiology and Epigenetics · DESanford Burnham Prebys Medical Discovery Institute · USUniversität Ulm · DEUniversity Hospital Ulm · DEUniversity Medical Center Freiburg · DEUniversity of Basel · CH

Funding

SPHINGOMYELIN SIGNALING PATHWAY IN FAS-INDUCED APOPTOSISP01CA069381 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 1996 to 2009
$16.8M
Lymphotoxin alpha Beta and LIGHT cytokine systemsR37AI033068 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2003 to 2012
$4.2M
SURFACE LYMPHOTOXIN A/B COMPLEXESR01AI033068 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI WARE, CARL F · 1994 to 2002
$1.0M
Human Lymphoid Tissue InducersR21AI088445 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2010 to 2011
$522k
NCI NIH HHS CA069381NCI NIH HHS P01 CA069381NIAID NIH HHS AI088445NIAID NIH HHS R01 AI033068NIAID NIH HHS R21 AI088445NIAID NIH HHS R37 AI033068NIAID NIH HHS R37AI033068
6 · The paper itself

Abstract

Whether the recently identified innate lymphocyte population coexpressing natural killer cell receptors (NKRs) and the nuclear receptor RORγt is part of the NK or lymphoid tissue inducer (LTi) cell lineage remains unclear. By using adoptive transfer of genetically tagged LTi-like cells, we demonstrate that NKR⁻RORγt(+) innate lymphocytes but not NK cells were direct progenitors to NKR(+)RORγt(+) cells in vivo. Genetic lineage tracing revealed that the differentiation of LTi-like cells was characterized by the stable upregulation of NKRs and a progressive loss of RORγt expression. Whereas interleukin-7 (IL-7) and intestinal microbiota stabilized RORγt expression within such NKR-LTi cells, IL-12 and IL-15 accelerated RORγt loss. RORγt(+) NKR-LTi cells produced IL-22, whereas RORγt⁻ NKR-LTi cells released IFN-γ and were potent inducers of colitis. Thus, the RORγt gradient in NKR-LTi cells serves as a tunable rheostat for their functional program. Our data also define a previously unappreciated role of RORγt⁻ NKR-LTi cells for the onset or maintenance of inflammatory bowel diseases.

Indexed as

AnimalsCell LineageDown-RegulationInflammatory Bowel DiseasesInterferon-gammaInterleukin-12Interleukin-15Interleukin-22Interleukin-7InterleukinsIntestinesKiller Cells, NaturalLymphocyte ActivationLymphoid TissueMiceMice, Inbred C57BLInterferon-gammaInterleukin-12Interleukin-15Interleukin-22Interleukin-7InterleukinsNuclear Receptor Subfamily 1, Group F, Member 3

Identifiers

PMID21093318
PMCPMC3042726
OpenAlexW2029529774

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.