Evidence map›Paper›PMID 30023182›Full record

ReviewJournal of microscopy and ultrastructure

Parasites-allergy paradox: Disease mediators or therapeutic modulators.

Mohammed A Afifi, Asif A Jiman-Fatani, Sherif El Saadany, Mahmoud A Fouad

Abstract readReview
In one paragraph

Review in Journal of microscopy and ultrastructure. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Mohammed A AfifiDepartment of Medical Microbiology and Parasitology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Asif A Jiman-FataniDepartment of Medical Microbiology and Parasitology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Sherif El SaadanyDepartment of Medical Microbiology and Parasitology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Mahmoud A FouadDepartment of Medical Microbiology and Parasitology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The noticeable phenomenon of an increased frequency of immune-inflammatory disorders, in the industrialized world, has led to the implication of parasitic infections in the pathophysiology of these diseases. Most of the studies investigated the infection connection to allergy have centered on helminthes. Parasitic helminthes are a group of metazoans that are evolutionary diverse, yet converge to evolve common modes of immunomodulation. Helminth immunoregulation is mainly mediated by a regulatory response including Treg and Breg cells with alternatively-activated macrophages. There is increasing evidence for a causal relationship between helminth infection and allergic hyporesponsiveness, however, conflicting data are still generating. The helminth immunoregulation seems to be species-specific and phase-specific. It depends on the stage of the clinical disease which correlates with a corresponding parasitic stage (egg, larva or mature adult). Here, we review the cellular and molecular mechanisms utilized by helminthes to manipulate the immune system and the consequent bystander immunomodulatory responses toward environmental allergens. We especially focus on parasitic species and molecules involved in the modulation of allergic disorders and summarize the experimental and clinical trials using them as therapeutic agents. We also discuss the potentials and obstacles, for helminthes and/or their derived molecules, to emerge as novel therapeutic modalities.

Indexed as

Allergic disordersHelminthsImmuneModulationParasites

Identifiers

PMID30023182
PMCPMC6014186

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.