Evidence map›Paper›PMID 24342422›Full record

ArticleCellular immunology2014

Selective CB2 receptor activation ameliorates EAE by reducing Th17 differentiation and immune cell accumulation in the CNS.

Weimin Kong, Hongbo Li, Ronald F Tuma, Doina Ganea

Open access · greenAbstract read
In one paragraph

Article in Cellular immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 93 citations in OpenAlex.

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  17. Cannabinoid-Based Medicines and Multiple Sclerosis.Advances in experimental medicine and biology · 2021
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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

4 authors at 1 institution in 1 country.

Weimin KongDepartment of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, United States.
Hongbo LiCenter for Substance Abuse Research and Department of Physiology, Temple University School of Medicine, Philadelphia, PA, United States.
Ronald F TumaCenter for Substance Abuse Research and Department of Physiology, Temple University School of Medicine, Philadelphia, PA, United States.
Doina GaneaDepartment of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, United States. Electronic address: dganea@temple.edu.
Temple University · US

Funding

Pilot Projects Core (PPC)P30DA013429 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI Anjali M Rajadhyaksha · 2000 to 2026
$34.6M
Training in Thrombosis, Hemostasis and Vascular BiologyT32HL007777 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KUNAPULI, SATYA P. · 1993 to 2012
$5.2M
CB2 Receptor Regulatin of Inflammatory Response in EAER01AI084065 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GANEA, DOINA, TUMA, RONALD F · 2009 to 2012
$1.5M
NHLBI NIH HHS 5T32HL007777-19NHLBI NIH HHS T32 HL007777NIAID NIH HHS 1R01 AI084065NIAID NIH HHS R01 AI084065NIDA NIH HHS P30 DA013429NIDA NIH HHS P30DA13429
6 · The paper itself

Abstract

CB2, the cannabinoid receptor expressed primarily on hematopoietic cells and activated microglia, mediates the immunoregulatory functions of cannabinoids. The involvement of CB2 in EAE has been demonstrated by using both endogenous and exogenous ligands. We showed previously that CB2 selective agonists inhibit leukocyte rolling and adhesion to CNS microvasculature and ameliorate clinical symptom in both chronic and remitting-relapsing EAE models. Here we showed that Gp1a, a highly selective CB2 agonist, with a four log higher affinity for CB2 than CB1, reduced clinical scores and facilitated recovery in EAE in conjunction with long term reduction in demyelination and axonal loss. We also established that Gp1a affected EAE through at least two different mechanisms, i.e. an early effect on Th1/Th17 differentiation in peripheral immune organs, and a later effect on the accumulation of pathogenic immune cells in the CNS, associated with reductions in the expression of CNS and T cell chemokine receptors, chemokines and adhesion molecules. This is the first report on the in vivo CB2-mediated Gp1a inhibition of Th17/Th1 differentiation. We also confirmed the Gp1a-induced inhibition of Th17/Th1 differentiation in vitro, both in non-polarizing and polarizing conditions. The CB2-induced inhibition of Th17 differentiation is highly relevant in view of recent studies emphasizing the importance of pathogenic self-reactive Th17 cells in EAE/MS. In addition, the combined effect on Th17 differentiation and immune cell accumulation into the CNS, emphasize the relevance of CB2 selective ligands as potential therapeutic agents in neuroinflammation.

Indexed as

AnimalsCell Adhesion MoleculesCell DifferentiationCell MovementCells, CulturedCentral Nervous SystemChemokinesDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalHumansIndenesMiceMice, Inbred C57BLMice, KnockoutMyelin-Oligodendrocyte GlycoproteinNeuroimmunomodulationCell Adhesion MoleculesChemokinesIndenesMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (34-56)N-(piperidin-1-yl)-1-(2,4-dichlorophenyl)-1,4-dihydro-6-methylindeno(1,2-c)pyrazole-3-carboxamidePeptide FragmentsPyrazolesReceptor, Cannabinoid, CB2Receptors, Chemokineantigen-presenting cellAPCBBBblood brain barrierCannabinoid receptorcannabinoid receptor 1cannabinoid receptor 2CB1CB2central nervous systemChemokinesCNSDCdendritic cellEAEexperimental autoimmune encephalomyelitisFACSfluorescence activated cell sorterGp1alipopolysaccharideLPSMNCsMOGmononuclear cellsMSmultiple sclerosismyelin oligodendrocyte glycoproteinPBSpertussis toxinphosphate buffered salinePTqRT-PCRquantitative RT-PCRT cell receptorTCRTh17 differentiation

Identifiers

PMID24342422
PMCPMC3906668
OpenAlexW2027446984

What OpenQuestion holds

Textmetadata
LicenceTDM
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.