Evidence map›Paper›PMID 26769487›Full record

ArticleNeuroscience bulletin2016

Programmed Death Ligand-1 on Microglia Regulates Th1 Differentiation via Nitric Oxide in Experimental Autoimmune Encephalomyelitis.

Jingxia Hu, Hao He, Zhengang Yang, Guangming Zhu, Li Kang, Xiuli Jing, Hai Lu, Wengang Song, Bo Bai, Hua Tang

Open access · bronzeAbstract read
In one paragraph

Article in Neuroscience bulletin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. CD8CNS neuroscience & therapeutics · 2024
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Glial Cell Expression of PD-L1.International journal of molecular sciences · 2019
    Review
  13. Reactive glia promote development of CD103Immunity, inflammation and disease · 2018
    Article
  14. Article
  15. Article
  16. 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

10 authors at 4 institutions in 1 country.

Jingxia HuCollege of Life Science, Shandong Agricultural University, Taian, 271018, China.
Hao HeInstitute of Immunology, Taishan Medical University, Taian, 271000, China.
Zhengang YangDepartment of ENT, Center Hospital of Taian City, Taian, 271000, China.
Guangming ZhuInstitute of Immunology, Taishan Medical University, Taian, 271000, China.
Li KangInstitute of Immunology, Taishan Medical University, Taian, 271000, China.
Xiuli JingInstitute of Immunology, Taishan Medical University, Taian, 271000, China.
Hai LuDepartment of Neurobiology, Jining Medical University, Jining, 272067, China.
Wengang SongInstitute of Immunology, Taishan Medical University, Taian, 271000, China.
Bo BaiDepartment of Neurobiology, Jining Medical University, Jining, 272067, China. bbai@mail.jnmc.edu.cn.
Hua TangInstitute of Immunology, Taishan Medical University, Taian, 271000, China. tanghuazhang218@163.com.
Taishan Medical University · CNJining Medical University · CNShandong Agricultural University · CNTaian City Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are considered to be potential antigen-presenting cells and have the ability to present antigen under pathological conditions. Nevertheless, whether and how microglia are involved in immune regulation are largely unknown. Here, we investigated the suppressive activity of microglia during experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein, with the goal of understanding their role in regulating the T cell reaction. Using flow cytometric analysis, we found that microglia were characterized by increased cell number and up-regulated programmed death ligand-1 (PD-L1) at the peak phase of EAE. Meanwhile, both the CD4(+) T cells and microglia that infiltrated the central nervous system expressed higher levels of PD1, the receptor for PD-L1, accompanied by a decline of Th1 cells. In an ex vivo co-culture system, microglia from EAE mice inhibited the proliferation of antigen-specific CD4(+) T cells and the differentiation of Th1 cells, and this was significantly inhibited by PD-L1 blockade. Further, microglia suppressed Th1 cells via nitric oxide (NO), the production of which was dependent on PD-L1. Thus, these data suggest a scenario in which microglia are involved in the regulation of EAE by suppressing Th1-cell differentiation via the PD-L1-NO pathway.

Indexed as

AnimalsB7-H1 AntigenCell DifferentiationEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryFluorescent Antibody TechniqueMiceMice, Inbred C57BLMice, TransgenicMicrogliaNitric OxidePolymerase Chain ReactionTh1 CellsB7-H1 AntigenCd274 protein, mouseNitric OxideEAEMicrogliaNegative immune regulationNitric oxidePD-L1

Identifiers

PMID26769487
PMCPMC5563746
OpenAlexW2467154812

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.