Immune Privilege: The Microbiome and Uveitis.
Animals
Bacteria
/ immunology
Blood-Brain Barrier
/ immunology
Dysbiosis
Gastrointestinal Microbiome
Genetic Predisposition to Disease
HLA-B27 Antigen
/ genetics
Humans
Immune Privilege
Intestines
/ microbiology
Risk Factors
T-Lymphocytes, Regulatory
/ immunology
Uvea
/ immunology
Uveitis
/ genetics
T regulatory cells
adjuvant effect
blood retinal barrier
commensals
folate
nutritional metabolites
probiotics
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
20
09
2020
accepted:
04
12
2020
entrez:
11
2
2021
pubmed:
12
2
2021
medline:
24
6
2021
Statut:
epublish
Résumé
Immune privilege (IP), a term introduced to explain the unpredicted acceptance of allogeneic grafts by the eye and the brain, is considered a unique property of these tissues. However, immune responses are modified by the tissue in which they occur, most of which possess IP to some degree. The eye therefore displays a spectrum of IP because it comprises several tissues. IP as originally conceived can only apply to the retina as it contains few tissue-resident bone-marrow derived myeloid cells and is immunologically shielded by a sophisticated barrier - an inner vascular and an outer epithelial barrier at the retinal pigment epithelium. The vascular barrier comprises the vascular endothelium and the glia limitans. Immune cells do not cross the blood-retinal barrier (BRB) despite two-way transport of interstitial fluid, governed by tissue oncotic pressure. The BRB, and the blood-brain barrier (BBB) mature in the neonatal period under signals from the expanding microbiome and by 18 months are fully established. However, the adult eye is susceptible to intraocular inflammation (uveitis; frequency ~200/100,000 population). Uveitis involving the retinal parenchyma (posterior uveitis, PU) breaches IP, while IP is essentially irrelevant in inflammation involving the ocular chambers, uveal tract and ocular coats (anterior/intermediate uveitis/sclerouveitis, AU). Infections cause ~50% cases of AU and PU but infection may also underlie the pathogenesis of immune-mediated "non-infectious" uveitis. Dysbiosis accompanies the commonest form, HLA-B27-associated AU, while latent infections underlie BRB breakdown in PU. This review considers the pathogenesis of uveitis in the context of IP, infection, environment, and the microbiome.
Identifiants
pubmed: 33569055
doi: 10.3389/fimmu.2020.608377
pmc: PMC7868421
doi:
Substances chimiques
HLA-B27 Antigen
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
608377Informations de copyright
Copyright © 2021 Mölzer, Heissigerova, Wilson, Kuffova and Forrester.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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