Evidence map›Paper›PMID 19400960›Full record

ArticleJournal of neuroinflammation2009

Functional interleukin-17 receptor A is expressed in central nervous system glia and upregulated in experimental autoimmune encephalomyelitis.

Jayasri Das Sarma, Bogoljub Ciric, Ryan Marek, Sanjoy Sadhukhan, Michael L Caruso, Jasmine Shafagh, Denise C Fitzgerald, Kenneth S Shindler, Am Rostami

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

102 citing papers in PubMed, 171 citations in OpenAlex.

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  7. Microglia and immune signaling as architects of the brain.Frontiers in cellular neuroscience · 2026
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42 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

9 authors at 3 institutions in 2 countries.

Jayasri Das SarmaDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. dassarmaj@iiserkol.ac.in
Bogoljub Ciric
Ryan Marek
Sanjoy Sadhukhan
Michael L Caruso
Jasmine Shafagh
Denise C Fitzgerald
Kenneth S Shindler
Am Rostami
Thomas Jefferson University · USIndian Institute of Science Education and Research Kolkata · INUniversity of Pennsylvania · US

Funding

The Role of Dendritic Cells in Intravenous ToleranceR01NS048435 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2004 to 2013
$2.9M
NINDS NIH HHS 5R01 NS048435NINDS NIH HHS R01 NS048435
6 · The paper itself

Abstract

backgroundInterleukin-17A (IL-17A) is the founding member of a novel family of inflammatory cytokines that plays a critical role in the pathogenesis of many autoimmune diseases, including multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). IL-17A signals through its receptor, IL-17RA, which is expressed in many peripheral tissues; however, expression of IL-17RA in the central nervous system (CNS) and its role in CNS inflammation are not well understood.

methodsEAE was induced in C57Bl/6 mice by immunization with myelin oligodendroglial glycoprotein. IL-17RA expression in the CNS was compared between control and EAE mice using RT-PCR, in situ hybridization, and immunohistochemistry. Cell-type specific expression was examined in isolated astrocytic and microglial cell cultures. Cytokine and chemokine production was measured in IL-17A treated cultures to evaluate the functional status of IL-17RA.

resultsHere we report increased IL-17RA expression in the CNS of mice with EAE, and constitutive expression of functional IL-17RA in mouse CNS tissue. Specifically, astrocytes and microglia express IL-17RA in vitro, and IL-17A treatment induces biological responses in these cells, including significant upregulation of MCP-1, MCP-5, MIP-2 and KC chemokine secretion. Exogenous IL-17A does not significantly alter the expression of IL-17RA in glial cells, suggesting that upregulation of chemokines by glial cells is due to IL-17A signaling through constitutively expressed IL-17RA.

conclusionIL-17RA expression is significantly increased in the CNS of mice with EAE compared to healthy mice, suggesting that IL-17RA signaling in glial cells can play an important role in autoimmune inflammation of the CNS and may be a potential pathway to target for therapeutic interventions.

Indexed as

Gene Expression RegulationAnimalsAnimals, NewbornCD11b AntigenCells, CulturedCentral Nervous SystemChemokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryGlial Fibrillary Acidic ProteinInterleukin-17MaleMiceMice, Inbred C57BLMyelin-Associated GlycoproteinCD11b AntigenChemokinesGlial Fibrillary Acidic ProteinInterleukin-17Mog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsReceptors, Interleukin-17RNA, Messenger

Identifiers

PMID19400960
PMCPMC2689857
OpenAlexW2090763524

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.