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2015 ; 11
(1
): 47-54
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Viral immune surveillance: Toward a TH17/TH9 gate to the central nervous system
#MMPMID25780281
Barkhordarian A
; Thames AD
; Du AM
; Jan AL
; Nahcivan M
; Nguyen MT
; Sama N
; Chiappelli F
Bioinformation
2015[]; 11
(1
): 47-54
PMID25780281
show ga
Viral cellular immune surveillance is a dynamic and fluid system that is driven
by finely regulated cellular processes including cytokines and other factors
locally in the microenvironment and systemically throughout the body. It is
questionable as to what extent the central nervous system (CNS) is an
immune-privileged organ protected by the blood-brain barrier (BBB). Recent
evidence suggests converging pathways through which viral infection, and its
associated immune surveillance processes, may alter the integrity of the
blood-brain barrier, and lead to inflammation, swelling of the brain parenchyma
and associated neurological syndromes. Here, we expand upon the recent "gateway
theory", by which viral infection and other immune activation states may disrupt
the specialized tight junctions of the BBB endothelium making it permeable to
immune cells and factors. The model we outline here builds upon the proposition
that this process may actually be initiated by cytokines of the IL-17 family, and
recognizing the intimate balance between TH17 and TH9 cytokine profiles
systemically. We argue that immune surveillance events, in response to viruses
such as the Human Immunodeficiency Virus (HIV), cause a TH17/TH9 induced gateway
through blood brain barrier, and thus lead to characteristic neuroimmune
pathology. It is possible and even probable that the novel TH17/TH9 induced
gateway, which we describe here, opens as a consequence of any state of immune
activation and sustained chronic inflammation, whether associated with viral
infection or any other cause of peripheral or central neuroinflammation. This
view could lead to new, timely and critical patient-centered therapies for
patients with neuroimmune pathologies across a variety of etiologies.
ABBREVIATIONS: BBB - blood brain barrier, BDV - Borna disease virus, CARD -
caspase activation and recruitment domains, CD - clusters of differentiation, CNS
- central nervous system, DAMP - damage-associated molecular patterns, DENV -
Dengue virus, EBOV - Ebola virus, ESCRT - endosomal sorting complex required for
transport-I, HepC - Hepatitis C virus, HIV - human immunodeficiency virus, IFN -
interferon, ILn - interleukin-n, IRF-n - interferon regulatory factor-n, MAVS -
mitochondrial antiviral-signaling, MBGV - Marburg virus, M-CSF - macrophage
colony-stimulating factor, MCP-1 - monocyte chemotactic protein 1 (aka CCL2), MHC
- major histocompatibility complex, MIP-? ? - macrophage inflammatory protein-1 ?
? (aka CCL3 & CCL4), MIF - macrophage migration inhibitory factor, NVE - Nipah
virus encephalitis, NK - natural killer cell, NLR - NLR, NOD - like receptor, NOD
- nucleotide oligomerization domain, PAMP - pathogen-associated molecular
patterns, PtdIns - phosphoinositides, PV - Poliovirus, RIG-I - retinoic
acid-inducible gene I, RIP - Receptor-interacting protein (RIP) kinase, RLR -
RIG-I-like receptor, sICAM1 - soluble intracellular adhesion molecule 1, STAT-3 -
signal tranducer and activator of transcription-3, sVCAM1 - soluble vascular cell
adhesion molecule 1, TANK - TRAF family member-associated NF- . B activator, TBK1
- TANK-binding kinase 1, TLR - Toll-like receptor, TNF - tumor necrosis factor,
TNFR - TNF receptor, TNFRSF21 - tumor necrosis factor receptor superfamily member
21, TRADD TNFR-SF1A - associated via death domain, TRAF TNFR - associated factor,
Tregs - regulatory T cellsubpopulation (CD4/8+CD25+FoxP3+), VHF - viral
hemorrhagic fever.