Evidence map›Paper›PMID 28617991›Full record

ArticleGlia2017

Interferon-β regulates the production of IL-10 by toll-like receptor-activated microglia.

Diogo Lobo-Silva, Guilhermina M Carriche, A Gil Castro, Susana Roque, Margarida Saraiva

Open access · bronzeAbstract read
In one paragraph

Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Extracellular vesicles from a novelFrontiers in immunology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Regulation of microglia polarization after cerebral ischemia.Frontiers in cellular neuroscience · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Biology and therapeutic potential of interleukin-10.The Journal of experimental medicine · 2020
    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

5 authors at 2 institutions in 1 country.

Diogo Lobo-SilvaLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.ORCID 0000-0002-9580-6618
Guilhermina M Carrichei3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
A Gil CastroLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Susana RoqueLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Margarida Saraivai3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.ORCID 0000-0002-8180-1293
University of Minho · PTUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pattern recognition receptors, such as toll-like receptors (TLRs), perceive tissue alterations and initiate local innate immune responses. Microglia, the resident macrophages of the brain, encode TLRs which primary role is to protect the tissue integrity. However, deregulated activation of TLRs in microglia may lead to chronic neurodegeneration. This double role of microglial responses is often reported in immune-driven neurologic diseases, as in multiple sclerosis (MS). Consequently, strategies to manipulate microglia inflammatory responses may help to ameliorate disease progression. In this context, the anti-inflammatory cytokine interleukin (IL)-10 appears as an attractive target. In this study, we investigated how activation of microglia by TLRs with distinct roles in MS impacts on IL-10 production. We found that activation of TLR2, TLR4, and TLR9 induced the production of IL-10 to a greater extent than activation of TLR3. This was surprising as both TLR3 and IL-10 play protective roles in animal models of MS. Interestingly, combination of TLR3 triggering with the other TLRs, enhanced IL-10 through the modulation of its transcription, via interferon (IFN)-β, but independently of IL-27. Thus, in addition to the modulation of inflammatory responses of the periphery described for the axis TLR3/IFN-β, we now report a direct modulation of microglial responses. We further show that the presence of IFN-γ in the microenvironment abrogated the modulation of IL-10 by TLR3, whereas that of IL-17 had no effect. Considering the therapeutic application of IFN-β in MS, our study bears important implications for the understanding of the cytokine network regulating microglia responses in this setting.

Indexed as

AnimalsCells, CulturedInterferon-betaInterleukin-10MacrophagesMice, Inbred C57BLMice, TransgenicMicrogliaMultiple SclerosisRNA, MessengerRNA StabilityToll-Like ReceptorsIL10 protein, mouseInterferon-betaInterleukin-10RNA, MessengerToll-Like Receptorsanti-inflammationcytokinesinnate immunitymultiple sclerosisneurodegeneration

Identifiers

PMID28617991
PMCPMC7165667
OpenAlexW2626423841

What OpenQuestion holds

Textmetadata
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.