Evidence map›Paper›PMID 24989828›Full record

ReviewImmunologic research2014

NLR proteins and parasitic disease.

Gwendolyn M Clay, Fayyaz S Sutterwala, Mary E Wilson

Abstract readReview
In one paragraph

Review in Immunologic research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
8.0field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Host genetic backgrounds: the key to determining parasite-host adaptation.Frontiers in cellular and infection microbiology · 2023
    Review
  10. Review
  11. The strategies of NLRP3 inflammasome to combatFrontiers in immunology · 2022
    Review
  12. Review
  13. Observational
  14. Article
  15. NLRP12 in innate immunity and inflammation.Molecular aspects of medicine · 2020
    Review
  16. Article
  17. Article
  18. Role of Alarmins in the Pathogenesis of Systemic Sclerosis.International journal of molecular sciences · 2020
    Review
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Gwendolyn M ClayThe Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa, 400 EMRB, 500 Newton Rd., Iowa City, IA, 52242, USA.
Fayyaz S Sutterwala
Mary E Wilson
University of Iowa · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
Immunogenetics of Leishmania chagasi InfectionR01AI048822 · NIAID · UNIVERSITY OF IOWA · PI WILSON, MARY EDYTHE · 2001 to 2005
$3.2M
Protective Immunity to Leishmania chagasiR01AI045540 · NIAID · UNIVERSITY OF IOWA · PI WILSON, MARY E · 2001 to 2011
$3.1M
Nlrp3 inflammasome signaling in immune responses to Candida albicansR01AI087630 · NIAID · UNIVERSITY OF IOWA · PI SUTTERWALA, FAYYAZ S. · 2010 to 2014
$1.8M
Genetic Risk Factors for Visceral LeishmaniasisR01AI076233 · NIAID · UNIVERSITY OF IOWA · PI BLACKWELL, JENEFER MARY, WILSON, MARY E · 2009 to 2013
$1.6M
The Role of Exosomes in the Pathogenesis of LeishmaniasisI01BX000536 · VA · IOWA CITY VA MEDICAL CENTER · PI WILSON, MARY E · 2009 to 2023
–
Innate inflammatory cells in leishmaniasisI01BX001983 · VA · IOWA CITY VA MEDICAL CENTER · PI WILSON, MARY E · 2014 to 2022
–
BLRD VA I01 BX000536BLRD VA I01 BX001983NIAID NIH HHS R01 AI045540NIAID NIH HHS R01 AI048822NIAID NIH HHS R01 AI076233NIAID NIH HHS R01 AI087630NIGMS NIH HHS T32 GM007337
6 · The paper itself

Abstract

Parasitic diseases are a serious global health concern. Many of the most common and most severe parasitic diseases, including Chagas' disease, leishmaniasis, and schistosomiasis, are also classified as neglected tropical diseases and are comparatively less studied than infectious diseases prevalent in high income nations. The NLRs (nucleotide-binding domain leucine-rich-repeat-containing proteins) are cytosolic proteins known to be involved in pathogen detection and host response. The role of NLRs in the host response to parasitic infection is just beginning to be understood. The NLR proteins NOD1 and NOD2 have been shown to contribute to immune responses during Trypanosoma cruzi infection, Toxoplasma gondii infection, and murine cerebral malaria. The NLRP3 inflammasome is activated by T. cruzi and Leishmania amazonensis but also induces pathology during infection with schistosomes or malaria. Both the NLRP1 and NLRP3 inflammasomes respond to T. gondii infection. The NLRs may play crucial roles in human immune responses during parasitic infection, usually acting as innate immune sensors and driving the inflammatory response against invading parasites. However, this inflammatory response can either kill the invading parasite or be responsible for destructive pathology. Therefore, understanding the role of the NLR proteins will be critical to understanding the host defense against parasites as well as the fine balance between homeostasis and parasitic disease.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsCarrier ProteinsHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinPortraits as TopicProtozoan InfectionsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCarrier ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP1 protein, humanNLRP3 protein, humanNLR ProteinsNOD1 protein, humanNod1 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID24989828
PMCPMC5106291
OpenAlexW1992113146

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.