Evidence map›Paper›PMID 31998072›Full record

ArticleFrontiers in molecular neuroscience2019

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis.

Chao Zheng, Jingtao Chen, Fengna Chu, Jie Zhu, Tao Jin

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Impact ofInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Investigations of remibrutinib in models pertinent to multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Frequency and Relevance of MYD88European journal of neurology · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Innate Immune Mechanisms in the Central Nervous System.Advances in experimental medicine and biology · 2025
    Review

14 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Chao ZhengDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Jingtao ChenInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Fengna ChuDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Jie ZhuDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Tao JinDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
First Hospital of Jilin University · CNJilin University · CNKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a neuro-autoimmune and neurodegenerative disorder leading to chronic inflammation, demyelination, axonal, and neuronal loss in the central nervous system (CNS). Despite intense research efforts, the pathogenesis of MS still remains unclear. Toll-like receptors (TLRs) are a family of type I transmembrane receptors that play a crucial role in the innate immune response. Myeloid differentiation factor 88 (MyD88) is the adaptor of major TLRs. It has been widely considered that the TLR-MyD88 signaling pathway plays an important role in the occurrence and development of autoimmune disease. Data have revealed that the TLR-MyD88 signaling may be involved in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), an animal model for MS, by regulating the antigen presentation of dendritic cells, the integrity of blood-brain barrier (BBB), and the activation of T cells and B cells. Here, we summarize the role of TLRs and MyD88 in MS and discuss the possible therapies that are based on these molecules.

Indexed as

experimental autoimmune encephalomyelitisinflammationmultiple sclerosismyeloid differentiation primary response protein 88Toll-like receptors

Identifiers

PMID31998072
PMCPMC6965019
OpenAlexW2999714040

What Socratic 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 Socratic graph.