Impaired regulatory T cell control of astroglial overdrive and microglial pruning in schizophrenia.
Neurosci Biobehav Rev
; 125: 637-653, 2021 06.
Article
in English
| MEDLINE | ID: covidwho-1126995
ABSTRACT
It is widely held that schizophrenia involves an active process of peripheral inflammation that induces or reflects brain inflammation with activation of microglia, the brain's resident immune cells. However, recent in vivo radioligand binding studies and large-scale transcriptomics in post-mortem brain report reduced markers of microglial inflammation. The findings suggest a contrary hypothesis; that microglia are diverted into their non-inflammatory synaptic remodelling phenotype that interferes with neurodevelopment and perhaps contributes to the relapsing nature of schizophrenia. Recent discoveries on the regulatory interactions between micro- and astroglial cells and immune regulatory T cells (Tregs) cohere with clinical omics data to suggest that i) disinhibited astrocytes mediate the shift in microglial phenotype via the production of transforming growth factor-beta, which also contributes to the disturbances of dopamine and GABA function in schizophrenia, and ii) systemically impaired functioning of Treg cells contributes to the dysregulation of glial function, the low-grade peripheral inflammation, and the hitherto unexplained predisposition to auto-immunity and reduced life-expectancy in schizophrenia, including greater COVID-19 mortality.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Schizophrenia
/
COVID-19
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Neurosci Biobehav Rev
Year:
2021
Document Type:
Article
Affiliation country:
J.neubiorev.2021.03.004
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