Evidence map›Paper›PMID 21847523›Full record

ArticleJournal of clinical immunology2011

Tyrosine kinase inhibitors ameliorate autoimmune encephalomyelitis in a mouse model of multiple sclerosis.

Oliver Crespo, Stacey C Kang, Richard Daneman, Tamsin M Lindstrom, Peggy P Ho, Raymond A Sobel, Lawrence Steinman, William H Robinson

Abstract read
In one paragraph

Article in Journal of clinical immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

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  17. Mast cells and angiogenesis in multiple sclerosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
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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

8 authors at 1 institution in 1 country.

Oliver CrespoDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Stacey C Kang
Richard Daneman
Tamsin M Lindstrom
Peggy P Ho
Raymond A Sobel
Lawrence Steinman
William H Robinson
Stanford University · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Tyrosine Kinase Pathways in Rheumatoid ArthritisR01AR054822 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI ROBINSON, WILLIAM H · 2007 to 2011
$1.5M
NHLBI NIH HHS N01-HV-00242NIAID NIH HHS 5 T32AI07290NIAID NIH HHS T32 AI007290NIAMS NIH HHS R01 AR-054822NIAMS NIH HHS R01 AR054822
6 · The paper itself

Abstract

Multiple sclerosis is an autoimmune disease of the central nervous system characterized by neuroinflammation and demyelination. Although considered a T cell-mediated disease, multiple sclerosis involves the activation of both adaptive and innate immune cells, as well as resident cells of the central nervous system, which synergize in inducing inflammation and thereby demyelination. Differentiation, survival, and inflammatory functions of innate immune cells and of astrocytes of the central nervous system are regulated by tyrosine kinases. Here, we show that imatinib, sorafenib, and GW2580-small molecule tyrosine kinase inhibitors-can each prevent the development of disease and treat established disease in a mouse model of multiple sclerosis. In vitro, imatinib and sorafenib inhibited astrocyte proliferation mediated by the tyrosine kinase platelet-derived growth factor receptor (PDGFR), whereas GW2580 and sorafenib inhibited macrophage tumor necrosis factor (TNF) production mediated by the tyrosine kinases c-Fms and PDGFR, respectively. In vivo, amelioration of disease by GW2580 was associated with a reduction in the proportion of macrophages and T cells in the CNS infiltrate, as well as a reduction in the levels of circulating TNF. Our findings suggest that GW2580 and the FDA-approved drugs imatinib and sorafenib have potential as novel therapeutics for the treatment of autoimmune demyelinating disease.

Indexed as

AnimalsAnisolesAstrocytesBenzamidesBenzenesulfonatesCell DifferentiationCell ProliferationCells, CulturedDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansImatinib MesylateMacrophagesMiceMice, Inbred C57BL5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamineAnisolesBenzamidesBenzenesulfonatesImatinib MesylateNiacinamidePhenylurea CompoundsPiperazinesProtein Kinase InhibitorsProtein-Tyrosine KinasesPyridinesPyrimidinesReceptor, Macrophage Colony-Stimulating FactorReceptors, Platelet-Derived Growth FactorSorafenibTumor Necrosis Factor-alpha

Identifiers

PMID21847523
PMCPMC3225802
OpenAlexW2123414173

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.