Evidence map›Paper›PMID 24927559›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Nod/Ripk2 signaling in dendritic cells activates IL-17A-secreting innate lymphoid cells and drives colitis in T-bet-/-.Rag2-/- (TRUC) mice.

Joerg Ermann, Tracy Staton, Jonathan N Glickman, Rene de Waal Malefyt, Laurie H Glimcher

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  13. [Regulation of ILC3/Th17-Mediated Intestinal Immune Response by Circadian Rhythm].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022
    Review
  14. Article
  15. RIPK protein kinase family: Atypical lives of typical kinases.Seminars in cell & developmental biology · 2021
    Review
  16. Article
  17. CUX1 and IκBζ (NFKBIZ) mediate the synergistic inflammatory response to TNF and IL-17A in stromal fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

5 authors at 4 institutions in 1 country.

Joerg ErmannDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA 02115;Harvard Medical School, Boston, MA 02115;
Tracy StatonDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115;
Jonathan N GlickmanDepartment of Pathology, Harvard Medical School, Boston, MA 02115;Miraca Life Sciences, Newton, MA 02464;
Rene de Waal MalefytBiologics Discovery, Merck Research Laboratories, Palo Alto, CA 94304; and.
Laurie H GlimcherWeill Cornell Medical College, New York, NY 10065 lglimche@med.cornell.edu.
Harvard University · USBrigham and Women's Hospital · USCornell University · USMerck & Co., Inc., Rahway, NJ, USA (United States) · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
T-bet and Tumor ImmunityR01CA112663 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GLIMCHER, LAURIE HOLLIS · 2005 to 2015
$3.3M
NCI NIH HHS CA112663NCI NIH HHS R01 CA112663NIDDK NIH HHS 5-P30 DK034854NIDDK NIH HHS P30 DK034854
6 · The paper itself

Abstract

T-bet(-/-).Rag2(-/-) (TRUC) mice spontaneously develop microbiota-driven, TNF-mediated large bowel inflammation that resembles human ulcerative colitis. We show here that IL-23 and IL-1-dependent secretion of IL-17A by innate lymphoid cells (ILCs; defined as CD45(+)lin(-)Thy1(hi)NKp46(-)) is a second critical pathway in this model. Using an in vitro coculture system of bone marrow-derived dendritic cells (DCs) and freshly isolated FACS-purified ILCs, we demonstrate that IL-23 and IL-1 secreted by DCs in response to microbial stimulation work together to induce IL-17A production by ILCs. TNF is not required for IL-17A secretion by ILCs in vitro but synergizes with IL-17A to induce the expression of neutrophil-attracting chemokines. Upstream, activation of the IL-23/IL-17A axis is regulated by nucleotide-binding oligomerization domain containing (Nod)/receptor-interacting serine-threonine kinase 2 (Ripk2) signals in DCs. Genetic ablation of the Nod/Ripk2 signaling pathway protects TRUC mice from developing colitis without affecting the colitogenicity of the intestinal microbiota. Our data provide insight into the complex network of interactions between IL-17A-secreting ILCs and other components of the innate immune system in the development of colitis.

Indexed as

AnimalsBacteriaBone Marrow CellsChemokinesColitis, UlcerativeDendritic CellsDNA-Binding ProteinsHumansInterleukin-17Interleukin-23IntestinesMiceMice, KnockoutReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesSignal TransductionChemokinesDNA-Binding ProteinsIl17a protein, mouseInterleukin-17Interleukin-23Rag2 protein, mouseReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouseT-bet Transcription FactorT-Box Domain Proteins

Identifiers

PMID24927559
PMCPMC4078823
OpenAlexW1984439354

What OpenQuestion holds

Textmetadata
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.