Evidence map›Paper›PMID 30166455›Full record

ReviewBioscience reports2018

Plasminogen-binding proteins as an evasion mechanism of the host's innate immunity in infectious diseases.

Dolores A Ayón-Núñez, Gladis Fragoso, Raúl J Bobes, Juan P Laclette

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The allergenic potential of enolases: physiological and pathophysiological insights.Current opinion in allergy and clinical immunology · 2025
    Review
  6. Article
  7. Glyceraldehyde 3-Phosphate Dehydrogenase on the Surface ofInternational journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. The Enolase of theInternational journal of molecular sciences · 2023
    Article
  11. Article
  12. Differential Protein Expression ofPathogens (Basel, Switzerland) · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Dolores A Ayón-NúñezDepartment of Immunology, Institute for Biomedical Research, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Gladis FragosoDepartment of Immunology, Institute for Biomedical Research, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Raúl J BobesDepartment of Immunology, Institute for Biomedical Research, Universidad Nacional Autónoma de México, Mexico City, Mexico laclette@biomedicas.unam.mx rbobes@biomedicas.unam.mx.
Juan P LacletteDepartment of Immunology, Institute for Biomedical Research, Universidad Nacional Autónoma de México, Mexico City, Mexico laclette@biomedicas.unam.mx rbobes@biomedicas.unam.mx.
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogens have developed particular strategies to infect and invade their hosts. Amongst these strategies' figures the modulation of several components of the innate immune system participating in early host defenses, such as the coagulation and complement cascades, as well as the fibrinolytic system. The components of the coagulation cascade and the fibrinolytic system have been proposed to be interfered during host invasion and tissue migration of bacteria, fungi, protozoa, and more recently, helminths. One of the components that has been proposed to facilitate pathogen migration is plasminogen (Plg), a protein found in the host's plasma, which is activated into plasmin (Plm), a serine protease that degrades fibrin networks and promotes degradation of extracellular matrix (ECM), aiding maintenance of homeostasis. However, pathogens possess Plg-binding proteins that can activate it, therefore taking advantage of the fibrin degradation to facilitate establishment in their hosts. Emergence of Plg-binding proteins appears to have occurred in diverse infectious agents along evolutionary history of host-pathogen relationships. The goal of the present review is to list, summarize, and analyze different examples of Plg-binding proteins used by infectious agents to invade and establish in their hosts. Emphasis was placed on mechanisms used by helminth parasites, particularly taeniid cestodes, where enolase has been identified as a major Plg-binding and activating protein. A new picture is starting to arise about how this glycolytic enzyme could acquire an entirely new role as modulator of the innate immune system in the context of the host-parasite relationship.

Indexed as

Bacterial ProteinsCarrier ProteinsCommunicable DiseasesExtracellular MatrixFibrinFibrinolysinFibrinolysisHost-Pathogen InteractionsHumansImmune EvasionImmunity, InnatePlasminogenProteolysisBacterial ProteinsCarrier ProteinsFibrinFibrinolysinPlasminogenplasminogen-binding protein, bacteriaenolasefibrinolytic systemhost/parasite relationshipimmune evasionPlasminogen

Identifiers

PMID30166455
PMCPMC6167496
OpenAlexW2889156744

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.