The immunologic etiology of psychiatric manifestations in systemic lupus erythematosus: A narrative review on the role of the blood brain barrier, antibodies, cytokines and chemokines.
Antibody
Blood-brain barrier
Chemokine
Cytokine
Neuropsychiatric systemic lupus erythematosus
Psychiatric
Journal
Autoimmunity reviews
ISSN: 1873-0183
Titre abrégé: Autoimmun Rev
Pays: Netherlands
ID NLM: 101128967
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
21
05
2020
accepted:
26
05
2020
pubmed:
21
6
2020
medline:
28
8
2020
entrez:
21
6
2020
Statut:
ppublish
Résumé
The aim of this narrative review is to provide an overview of the literature on the possible immunologic pathophysiology of psychiatric manifestations of neuropsychiatric systemic lupus erythematosus (NPSLE). A systematic search on PubMed was conducted. English studies with full text availability that investigated the correlation between blood-brain barrier (BBB) dysfunction, intrathecal synthesis of antibodies, antibodies, cytokines, chemokines, metalloproteinases, complement and psychiatric NPSLE manifestations in adults were included. Both transient BBB-dysfunction with consequent access of antibodies to the cerebrospinal fluid (CSF) and intrathecal synthesis of antibodies could occur in psychiatric NPSLE. Anti-phospholipid antibodies, anti-NMDA antibodies and anti-ribosomal protein p antibodies seem to mediate concentration dependent neuronal dysfunction. Interferon-α may induce microglial engulfment of neurons, direct neuronal damage and production of cytokines and chemokines in psychiatric NPSLE. Several cytokines, chemokines and matrix metalloproteinase-9 may contribute to the pathophysiology of psychiatric NPSLE by attracting and activating Th1-cells and B-cells. This potential pathophysiology may help understand NPSLE and may have implications for the diagnostic management and therapy of psychiatric NPSLE. However, the presented pathophysiological model is based on correlations between potential immunologic etiologies and psychiatric NPSLE that remain questionable. More research on this topic is necessary to further elucidate the pathophysiology of NPSLE.
Identifiants
pubmed: 32561462
pii: S1568-9972(20)30156-7
doi: 10.1016/j.autrev.2020.102592
pii:
doi:
Substances chimiques
Antibodies
0
Chemokines
0
Cytokines
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
102592Informations de copyright
Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest No conflicts of interest were stated. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.