Evidence map›Paper›PMID 33308135›Full record

ArticleBMC bioinformatics2020

Computational modeling of the immune response in multiple sclerosis using epimod framework.

Simone Pernice, Laura Follia, Alessandro Maglione, Marzio Pennisi, Francesco Pappalardo, Francesco Novelli, Marinella Clerico, Marco Beccuti, Francesca Cordero, Simona Rolla

Open access · goldAbstract read
In one paragraph

Article in BMC bioinformatics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 20 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Simone PerniceDepartment of Computer Science, University of Turin, Turin, Italy.
Laura FolliaDepartment of Computer Science, University of Turin, Turin, Italy.
Alessandro MaglioneDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Marzio PennisiComputer Science Inst., DiSIT, University of Eastern Piedmont, Alessandria, Italy.
Francesco PappalardoDepartment of Drug Sciences, University of Catania, Catania, Italy.
Francesco NovelliDepartment of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
Marinella ClericoDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Marco BeccutiDepartment of Computer Science, University of Turin, Turin, Italy. marco.beccuti@unito.it.ORCID http://orcid.org/0000-0001-6125-9460
Francesca CorderoDepartment of Computer Science, University of Turin, Turin, Italy.
Simona RollaDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
University of Turin · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Catania · IT

Funding

Fondazione CRT 2019.2292Fondi di Ricerca Locale, Univ. degli Studi di Torino BECM_RILO_19_01
6 · The paper itself

Abstract

backgroundMultiple Sclerosis (MS) represents nowadays in Europe the leading cause of non-traumatic disabilities in young adults, with more than 700,000 EU cases. Although huge strides have been made over the years, MS etiology remains partially unknown. Furthermore, the presence of various endogenous and exogenous factors can greatly influence the immune response of different individuals, making it difficult to study and understand the disease. This becomes more evident in a personalized-fashion when medical doctors have to choose the best therapy for patient well-being. In this optics, the use of stochastic models, capable of taking into consideration all the fluctuations due to unknown factors and individual variability, is highly advisable.

resultsWe propose a new model to study the immune response in relapsing remitting MS (RRMS), the most common form of MS that is characterized by alternate episodes of symptom exacerbation (relapses) with periods of disease stability (remission). In this new model, both the peripheral lymph node/blood vessel and the central nervous system are explicitly represented. The model was created and analysed using Epimod, our recently developed general framework for modeling complex biological systems. Then the effectiveness of our model was shown by modeling the complex immunological mechanisms characterizing RRMS during its course and under the DAC administration.

conclusionsSimulation results have proven the ability of the model to reproduce in silico the immune T cell balance characterizing RRMS course and the DAC effects. Furthermore, they confirmed the importance of a timely intervention on the disease course.

Indexed as

Models, BiologicalUser-Computer InterfaceAlgorithmsDaclizumabHumansImmune SystemImmunosuppressive AgentsMultiple Sclerosis, Relapsing-RemittingStochastic ProcessesDaclizumabImmunosuppressive AgentsComputational modelingImmune systemMultiple sclerosisPetri netStochastic modeling

Identifiers

PMID33308135
PMCPMC7734848
OpenAlexW3111610496

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.