Evidence map›Paper›PMID 21251876›Full record

ArticleTrends in immunology2011

The ever-expanding function of NOD2: autophagy, viral recognition, and T cell activation.

Michael H Shaw, Nobuhiko Kamada, Neil Warner, Yun-Gi Kim, Gabriel Nuñez

Open access · greenAbstract read
In one paragraph

Article in Trends in immunology, 2011. 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
5.0field-weighted citation impact, top 4% 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, 82 citations in OpenAlex.

  1. Deciphering the Implications ofPathogens (Basel, Switzerland) · 2026
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  16. Molecular Interactions of Autophagy with the Immune System and Cancer.International journal of molecular sciences · 2017
    Review
  17. Review
  18. Article
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  20. NOD2 induces autophagy to control AIEC bacteria infectiveness in intestinal epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    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

5 authors at 1 institution in 1 country.

Michael H ShawDepartment of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Nobuhiko Kamada
Neil Warner
Yun-Gi Kim
Gabriel Nuñez
University of Michigan–Ann Arbor · US

Funding

Lung Immunopathology Training Stipend SupplementT32HL007517 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1985 to 2022
$6.1M
Nod2: A Susceptibility Gene for Crohn's DiseaseR01DK061707 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2002 to 2017
$4.7M
Cryopyrin/NLRP3 Signaling in Inflammation and Innate ImmunityR37AI063331 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2016 to 2025
$3.9M
Cryopyrin Signaling in Inflammation and Innate ImmunityR01AI063331 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2005 to 2015
$3.3M
The Role of Inflammasomes in Mucosal Immunity to Intestinal Bacterial PathogensR01DK091191 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2010 to 2019
$3.1M
Role of Mast Cells in NLRP3-Mediated Skin InflammationR01AR059688 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2010 to 2014
$1.7M
Role of ASC signaling Pathway in Inflammatory DiseaseR01AR052756 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2006 to 2010
$1.4M
Cryopyrin/NLRP3 Signaling in Inflammation and Innate ImmunityR56AI063331 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2010 to 2010
$386k
NHLBI NIH HHS 2T32 HL007517NHLBI NIH HHS T32 HL007517NIAID NIH HHS AI063331NIAID NIH HHS R01 AI063331NIAID NIH HHS R37 AI063331NIAID NIH HHS R56 AI063331NIAMS NIH HHS AR051790NIAMS NIH HHS AR059688NIAMS NIH HHS R01 AR052756NIAMS NIH HHS R01 AR059688NIDDK NIH HHS DK091191NIDDK NIH HHS DK61707NIDDK NIH HHS R01 DK061707NIDDK NIH HHS R01 DK091191
6 · The paper itself

Abstract

The identification of several families of innate pattern recognition receptors has greatly enhanced our understanding of the host innate immune response against a variety of pathogens. One such family of innate receptors is the nucleotide-binding domain and leucine rich repeat containing receptors (NLRs). NOD2 has been characterized as a cytosolic sensor of bacteria peptidoglycan (PGN). For almost 10 years, NOD2 was assigned with the function of mediating the RICK- and nuclear factor-κB induced proinflammatory response triggered by PGN. Recent studies have extended the biological activity of NOD2 to include the induction of autophagy and antiviral responses, as well as mediating direct T cell activation. Here, we highlight and discuss these new findings in the context of immune activation and pathogen detection.

Indexed as

AutophagyLymphocyte ActivationAdaptive ImmunityAnimalsHumansNod2 Signaling Adaptor ProteinT-LymphocytesNod2 Signaling Adaptor Protein

Identifiers

PMID21251876
PMCPMC3056277
OpenAlexW2160384091

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.