Evidence map›Paper›PMID 28681705›Full record

ArticleBMC immunology2017

A model of auto immune response.

James K Peterson, Alison M Kesson, Nicholas J C King

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. AnACS omega · 2026
    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.

James K PetersonDepartment of Biological Sciences, Department of Mathematical Sciences, Clemson University, Martin Hall O-304, BOX 340975, Clemson, 340975, SC, USA. petersj@clemson.edu.
Alison M KessonDiscipline of Child and Adolescent Health and the Marie Bashir Institute for Emerging Infectious Diseases and Biosecurity, University of Sydney, Sydney, NSW, Australia.
Nicholas J C KingDiscipline of Pathology, University of Sydney, Sydney, NSW, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn this work, we develop a theoretical model of an auto immune response. This is based on modifications of standard second messenger trigger models using both signalling pathways and diffusion and a macro level dynamic systems approximation to the response of a triggering agent such as a virus, bacteria or environmental toxin.

resultsWe show that there, in general, will be self damage effects whenever the triggering agent's effect on the host can be separated into two distinct classes of cell populations. In each population, the trigger acts differently and this behavior is mediated by the nonlinear interactions between two signalling agents.

conclusionIf these interactions satisfy certain critical assumptions this will lead to collateral damage. If the initial triggering agent's action involves any critical host cell population whose loss can lead to serious host health issues, then there is a much increased probability of host death. Our model also shows that if the nonlinear interaction assumptions are satisfied, there is a reasonable expectation of oscillatory behavior in host health; i.e. periods of remission.

Indexed as

Immunity, CellularModels, ImmunologicalAnimalsBacteriaHumansSecond Messenger SystemsToxins, BiologicalVirusesToxins, BiologicalAbstract triggering agentAuto immune responsesHost self damage and deathOscillation in health levels and remissionSecond messenger modelsSignalling agent mediation

Identifiers

PMID28681705
PMCPMC5499147

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.