Evidence map›Paper›PMID 32721043›Full record

ReviewImmunological reviews2020

The pyrin inflammasome and the Yersinia effector interaction.

Haleema S Malik, James B Bliska

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. ThebioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review
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.

Haleema S MalikDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA.ORCID 0000-0003-0780-5509
James B BliskaDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA.ORCID 0000-0002-6047-8837
Dartmouth College · US

Funding

Regulation of host innate and adaptive immunity by bacterial type III effectorsR01AI099222 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BLISKA, JAMES B · 2012 to 2025
$5.9M
NIAID NIH HHS R01 AI099222
6 · The paper itself

Abstract

Pyrin is a cytosolic pattern-recognition receptor that normally functions as a guard to trigger capase-1 inflammasome assembly in response to bacterial toxins and effectors that inactivate RhoA. The MEFV gene encoding human pyrin is preferentially expressed in phagocytes. Key domains in pyrin include a pyrin domain (PYD), a linker region, and a B30.2 domain. Binding of ASC to pyrin by a PYD-PYD interaction triggers inflammasome assembly. Pyrin is held in an inactive conformation by negative regulation mechanisms to avoid premature inflammasome assembly. One mechanism of negative regulation involves phosphorylation of the linker by PRK kinase which in turn is positively regulated by active RhoA. The B30.2 domain also negatively regulates pyrin. Gain of function mutations in MEFV responsible for the autoinflammatory disease Familial Mediterranean Fever (FMF) map to exon 10 encoding the B30.2 domain. Insights into pyrin regulation have come from studies of several Yersinia effectors, which are injected into phagocytes and interact with the RhoA-PRK-pyrin axis during infection. Two effectors, YopE and YopT, inactivate RhoA to disrupt phagocytic signaling. To counteract an effector-triggered immune response, a third effector, YopM, binds to and inhibits pyrin by hijacking PRK and RSK and directing linker phosphorylation. Inhibition of pyrin by YopM is required for virulence of Yersinia pestis, the agent of plague. Recent results from infection studies with human phagocytes and mice producing pyrin B30.2 FMF variants show that gain of function MEFV mutations bypass inhibition by YopM. Population genetic data suggest that MEFV mutations were selected for in individuals of Mediterranean decent during historic plague pandemics. This review discusses current concepts of pyrin regulation and its interaction with Yersinia effectors.

Indexed as

Bacterial ToxinsFamilial Mediterranean FeverAnimalsInflammasomesMiceMutationPyrinYersiniaBacterial ToxinsInflammasomesMefv protein, mousePyrineffectorFamilial Mediterranean FeverinflammasomePyrinRhoAYersinia

Identifiers

PMID32721043
PMCPMC7989412
OpenAlexW3045795522

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.