Evidence map›Paper›PMID 29104236›Full record

ReviewInternational journal of molecular sciences2017

The Emerging Role of the Major Histocompatibility Complex Class I in Amyotrophic Lateral Sclerosis.

Gabriela Bortolança Chiarotto, Giovanni Nardo, Maria Chiara Trolese, Marcondes Cavalcante França, Caterina Bendotti, Alexandre Leite Rodrigues de Oliveira

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Phenotypic heterogeneity of astrocytes in motor neuron disease.Clinical & experimental neuroimmunology · 2018
    Review
  8. Counteracting roles of MHCI and CD8Molecular neurodegeneration · 2018
    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

6 authors at 2 institutions in 2 countries.

Gabriela Bortolança ChiarottoDepartment of Structural and Functional Biology, Institute of Biology-Unicamp, 13083-865 Campinas, Brazil. gabrielachiarotto@gmail.com.
Giovanni NardoDepartment of Neuroscience, IRCCS-Institute of Pharmacological Research Mario Negri, 20156 Milano, Italy. giovanni.nardo@marionegri.it.ORCID 0000-0002-1803-1484
Maria Chiara TroleseDepartment of Neuroscience, IRCCS-Institute of Pharmacological Research Mario Negri, 20156 Milano, Italy. mariachiara.trolese@marionegri.it.
Marcondes Cavalcante FrançaDepartament of Neurology, Faculty of Medical Sciences-Unicamp, 13083-887 Campinas, Brazil. mcfrancajr@uol.com.br.
Caterina BendottiDepartment of Neuroscience, IRCCS-Institute of Pharmacological Research Mario Negri, 20156 Milano, Italy. caterina.bendotti@marionegri.it.
Alexandre Leite Rodrigues de OliveiraDepartment of Structural and Functional Biology, Institute of Biology-Unicamp, 13083-865 Campinas, Brazil. alroliv@unicamp.br.ORCID 0000-0003-4224-4575
Mario Negri Institute for Pharmacological Research · ITUniversidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting upper and lower motoneurons (MNs). The etiology of the disease is still unknown for most patients with sporadic ALS, while in 5-10% of the familial cases, several gene mutations have been linked to the disease. Mutations in the gene encoding Cu, Zn superoxide dismutase (SOD1), reproducing in animal models a pathological scenario similar to that found in ALS patients, have allowed for the identification of mechanisms relevant to the ALS pathogenesis. Among them, neuroinflammation mediated by glial cells and systemic immune activation play a key role in the progression of the disease, through mechanisms that can be either neuroprotective or neurodetrimental depending on the type of cells and the MN compartment involved. In this review, we will examine and discuss the involvement of major histocompatibility complex class I (MHCI) in ALS concerning its function in the adaptive immunity and its role in modulating the neural plasticity in the central and peripheral nervous system. The evidence indicates that the overexpression of MHCI into MNs protect them from astrocytes' toxicity in the central nervous system (CNS) and promote the removal of degenerating motor axons accelerating collateral reinnervation of muscles.

Indexed as

Adaptive ImmunityAmyotrophic Lateral SclerosisAnimalsHistocompatibility Antigens Class IHumansMicrogliaNeurogliaNeuronal PlasticityNeuroprotectionHistocompatibility Antigens Class Iamyotrophic lateral sclerosisglial cellsmajor histocompatibility complex Imicroglianeuroprotection

Identifiers

PMID29104236
PMCPMC5713268
OpenAlexW2766549629

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.