Evidence map›Paper›PMID 26216406›Full record

ArticleExperimental and molecular pathology2015

IL-9 signaling affects central nervous system resident cells during inflammatory stimuli.

Xiaoli Ding, Fang Cao, Langjun Cui, Bogoljub Ciric, Guang-Xian Zhang, Abdolmohamad Rostami

Open access · greenAbstract read
In one paragraph

Article in Experimental and molecular pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-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

32 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  16. The Exposure to Lead (Pb) Exacerbates Immunological Abnormalities in BTBR TInternational journal of molecular sciences · 2023
    Article
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  18. A glance through the effects of CD4Computational and structural biotechnology journal · 2023
    Review
  19. Article
  20. 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 3 institutions in 2 countries.

Xiaoli DingDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA; Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Fang CaoXijing Hospital of Digestive Diseases, The Fourth Military Medical University, Xi'an 710032, China.
Langjun CuiKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Bogoljub CiricDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Guang-Xian ZhangDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Abdolmohamad RostamiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: a.m.rostami@jefferson.edu.
Thomas Jefferson University · USShaanxi Normal University · CNXijing Hospital · CN

Funding

NSCs produce a triply effective cocktail in the CNS for MS/EAE therapyR01NS075260 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, GUANG-XIAN · 2012 to 2016
$1.5M
NINDS NIH HHS R01 NS075260
6 · The paper itself

Abstract

Interleukin (IL) 9, a dominant cytokine in Th9 cells, has been proven to play a pathogenic role in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by augmenting T cell activation and differentiation; however, whether IL-9 signaling affects central nervous system (CNS)-resident cells during CNS autoimmunity remains unknown. In the present study, we found that the IL-9 receptor (IL-9R) was highly expressed in astrocytes, oligodendrocyte progenitor cells (OPCs), oligodendrocytes and microglia cells, and that its expression was significantly upregulated in brain and spinal cord during EAE. In addition, IL-9 increased chemokine expression, including CXCL9, CCL20 and MMP3, in primary astrocytes. Although IL-9 had no effect on the proliferation of microglia cells, it decreased OPC proliferation and differentiation when in combination with other pro-inflammatory cytokines, but not with IFN-γ. IL-9 plus IFN-γ promoted OPC proliferation and differentiation. These findings indicate that CNS-restricted IL-9 signaling may be involved in the pathogenesis of MS/EAE, thus providing a potential therapeutic target for future MS/EAE treatment through disruption of CNS cell-specific IL-9 signaling.

Indexed as

AnimalsAstrocytesAutoimmunityEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunohistochemistryInflammationInterleukin-9Lymphocyte ActivationMiceMice, Inbred C57BLMicrogliaNeurogliaOligodendrogliaReal-Time Polymerase Chain ReactionReceptors, Interleukin-9Il9r protein, mouseInterleukin-9Receptors, Interleukin-9CNS resident cellsExperimental autoimmune encephalomyelitisIL-9IL-9 receptor

Identifiers

PMID26216406
PMCPMC6524950
OpenAlexW1035302579

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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.