IL-17A is associated with the breakdown of the blood-brain barrier in relapsing-remitting multiple sclerosis.
Adult
Aged
Animals
Blood-Brain Barrier
Cells, Cultured
Encephalomyelitis, Autoimmune, Experimental
/ physiopathology
Endothelial Cells
/ drug effects
Female
Humans
Immunization, Passive
Interleukin-17
/ antagonists & inhibitors
Interleukin-6
/ pharmacology
Mice
Mice, Inbred C57BL
Middle Aged
Multiple Sclerosis, Relapsing-Remitting
/ cerebrospinal fluid
Receptors, Interleukin-6
/ physiology
Recombinant Proteins
/ pharmacology
Young Adult
Journal
Journal of neuroimmunology
ISSN: 1872-8421
Titre abrégé: J Neuroimmunol
Pays: Netherlands
ID NLM: 8109498
Informations de publication
Date de publication:
15 07 2019
15 07 2019
Historique:
received:
24
12
2018
revised:
18
04
2019
accepted:
19
04
2019
pubmed:
30
4
2019
medline:
31
3
2020
entrez:
30
4
2019
Statut:
ppublish
Résumé
IL-17 has been implicated in the pathogenesis of multiple sclerosis (MS). Here, we show that blockade of IL-17A, but not IL-17F, attenuated experimental autoimmune encephalomyelitis (EAE). We further show that IL-17A levels were elevated in the CSF of relapsing-remitting MS (RRMS) patients and that they correlated with the CSF/serum albumin quotient (Qalb), a measure of blood-brain barrier (BBB) dysfunction. We then demonstrated that the combination of IL-17A and IL-6 reduced the expression of tight junction (TJ)-associated genes and disrupted monolayer integrity in the BBB cell line hCMEC/D3. However, unlike IL-17A, IL-6 in the CSF from RRMS patients did not correlate with Qalb. These data highlight the potential importance of targeting IL-17A in preserving BBB integrity in RRMS.
Identifiants
pubmed: 31034962
pii: S0165-5728(18)30579-4
doi: 10.1016/j.jneuroim.2019.04.011
pii:
doi:
Substances chimiques
IL17A protein, human
0
IL17F protein, human
0
IL6 protein, human
0
Il17a protein, mouse
0
Interleukin-17
0
Interleukin-6
0
Receptors, Interleukin-6
0
Recombinant Proteins
0
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
147-154Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.