Show simple item record

dc.creatorDimitrijević, Mirjana
dc.creatorMitić, Katarina
dc.creatorKuštrimović, Nataša
dc.creatorVujić, Vesna
dc.creatorStanojević, Stanislava
dc.date.accessioned2021-02-18T10:39:12Z
dc.date.available2021-02-18T10:39:12Z
dc.date.issued2012
dc.identifier.issn0165-5728
dc.identifier.urihttp://intor.torlakinstitut.com/handle/123456789/357
dc.description.abstractNeuropeptide Y (NPY) suppressed clinical experimental autoimmune encephalomyelitis (EAE) and reduced numbers of CD28+, CD11b+ and CD80+ cells among spinal cord infiltrating cells at the peak of disease in Dark Agouti rat strain. Suppression of EAE was accompanied by the reduced expression of costimulatory CD80 and CD86 molecules on ED1+ macrophages and OX62+ dendritic cells in draining lymph nodes during the inductive phase of EAE. An inhibitor of dipeptidyl peptidase 4, an enzyme which terminates the action of NPY on 11 receptor subtype, did not sustain the suppressive effect of NPY on the EAE development, suggesting involvement of Y2 and Y5 receptors. (C) 2012 Elsevier B.V. All rights reserved.en
dc.publisherElsevier, Amsterdam
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175050/RS//
dc.rightsrestrictedAccess
dc.sourceJournal of Neuroimmunology
dc.subjectEAEen
dc.subjectDipeptidyl peptidase 4en
dc.subjectNeuropeptide Yen
dc.subjectRaten
dc.titleNPY suppressed development of experimental autoimmune encephalomyelitis in Dark Agouti rats by disrupting costimulatory molecule interactionsen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage31
dc.citation.issue1-2
dc.citation.other245(1-2): 23-31
dc.citation.rankM22
dc.citation.spage23
dc.citation.volume245
dc.identifier.doi10.1016/j.jneuroim.2012.01.013
dc.identifier.pmid22365383
dc.identifier.rcubconv_291
dc.identifier.scopus2-s2.0-84859644108
dc.identifier.wos000303908100004
dc.type.versionpublishedVersion


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record