Evidence map›Paper›PMID 32838963›Full record

ReviewMolecular aspects of medicine2020

NLRP12 in innate immunity and inflammation.

Shraddha Tuladhar, Thirumala-Devi Kanneganti

Open access · greenAbstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 144 citations in OpenAlex.

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  15. PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025
    Review
  16. The molecular mechanisms and therapeutic implications of PANoptosis in ischemic diseases.Apoptosis : an international journal on programmed cell death · 2025
    Review
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22 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Shraddha TuladharDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA. Electronic address: Thirumala-Devi.Kanneganti@StJude.org.
St. Jude Children's Research Hospital · US

Funding

Innate immune sensors, inflammasomes, and inflammasome-mediated processes in cancerR35CA253095 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2020 to 2026
$7.0M
Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
Targeting innate immune pathways, and inflammatory cell death in cytokine-mediated diseasesR01AI160179 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2021 to 2025
$4.2M
NLR signaling in colitis and colorectal tumorigenesisR01CA163507 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2020
$3.5M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS R01 CA163507NCI NIH HHS R35 CA253095NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R01 AI160179NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

Nucleotide-binding leucine-rich repeat-containing proteins, or NOD-like receptors (NLRs), are intracellular innate immune sensors that can regulate several signaling pathways, including MyD88- and TRIF-dependent pathways. In addition to these regulatory roles, some NLRs can assemble into multimeric protein complexes known as inflammasomes. NLRP12 is a member of the NLR family that contains an N-terminal pyrin domain, a central nucleotide-binding domain, and a C-terminal leucine-rich repeat. It has been shown to play a role in forming an inflammasome in response to specific infections, and it can also function as a regulator of inflammatory signaling. During Yersinia pestis or Plasmodium chabaudi infection, NLRP12 induces the release of the inflammasome-dependent cytokines IL-1β and IL-18. These NLRP12-dependent cytokines confer protection against severe infections caused by these pathogens. Conversely, during infection with Salmonella enterica serovar Typhimurium, vesicular stomatitis virus, Klebsiella pneumoniae, or Mycobacterium tuberculosis, and in colonic tumorigenesis, NLRP12 acts as a negative regulator of the NFκB and MAPK signaling pathways. NLRP12 also negatively regulates canonical and non-canonical signaling in T cells and causes exacerbated autoimmune diseases. Furthermore, NLRP12 acts as a central component in maintaining intestinal inflammation and gut homeostasis. Therefore, the ability of NLRP12 to function as an inflammasome or as a negative regulator is context-dependent. In this review, we provide an overview of the NLR family members and summarize recent insights into the roles of NLRP12 as an inflammasome and as a negative regulator.

Indexed as

Immunity, InnateInflammasomesHumansInflammationIntracellular Signaling Peptides and ProteinsNF-kappa BSignal TransductionInflammasomesIntracellular Signaling Peptides and ProteinsNF-kappa BNLRP12 protein, humanASCCancerCaspase-1Cell deathGasderminIL-18IL-1βInfectionInflammasomeInflammationNegative regulatorNLRP12Pyrin domainPyroptosis

Identifiers

PMID32838963
PMCPMC9375713
OpenAlexW3080129151

What OpenQuestion holds

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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.