Neuropeptide 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.
Keywords:
EAE / Dipeptidyl peptidase 4 / Neuropeptide Y / Rat
TY - JOUR
AU - Dimitrijević, Mirjana
AU - Mitić, Katarina
AU - Kuštrimović, Nataša
AU - Vujić, Vesna
AU - Stanojević, Stanislava
PY - 2012
UR - http://intor.torlakinstitut.com/handle/123456789/357
AB - Neuropeptide 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.
PB - Elsevier, Amsterdam
T2 - Journal of Neuroimmunology
T1 - NPY suppressed development of experimental autoimmune encephalomyelitis in Dark Agouti rats by disrupting costimulatory molecule interactions
EP - 31
IS - 1-2
SP - 23
VL - 245
DO - 10.1016/j.jneuroim.2012.01.013
ER -
@article{
author = "Dimitrijević, Mirjana and Mitić, Katarina and Kuštrimović, Nataša and Vujić, Vesna and Stanojević, Stanislava",
year = "2012",
url = "http://intor.torlakinstitut.com/handle/123456789/357",
abstract = "Neuropeptide 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.",
publisher = "Elsevier, Amsterdam",
journal = "Journal of Neuroimmunology",
title = "NPY suppressed development of experimental autoimmune encephalomyelitis in Dark Agouti rats by disrupting costimulatory molecule interactions",
pages = "31-23",
number = "1-2",
volume = "245",
doi = "10.1016/j.jneuroim.2012.01.013"
}
Dimitrijević, M., Mitić, K., Kuštrimović, N., Vujić, V.,& Stanojević, S. (2012). NPY suppressed development of experimental autoimmune encephalomyelitis in Dark Agouti rats by disrupting costimulatory molecule interactions.
Journal of Neuroimmunology
Elsevier, Amsterdam., 245(1-2), 23-31.
https://doi.org/10.1016/j.jneuroim.2012.01.013
Dimitrijević M, Mitić K, Kuštrimović N, Vujić V, Stanojević S. NPY suppressed development of experimental autoimmune encephalomyelitis in Dark Agouti rats by disrupting costimulatory molecule interactions. Journal of Neuroimmunology. 2012;245(1-2):23-31
Dimitrijević Mirjana, Mitić Katarina, Kuštrimović Nataša, Vujić Vesna, Stanojević Stanislava, "NPY suppressed development of experimental autoimmune encephalomyelitis in Dark Agouti rats by disrupting costimulatory molecule interactions" Journal of Neuroimmunology, 245, no. 1-2 (2012):23-31,
https://doi.org/10.1016/j.jneuroim.2012.01.013 .
