Molecular Brain,
Journal Year:
2024,
Volume and Issue:
17(1)
Published: Jan. 23, 2024
Abstract
The
central
nervous
system
(CNS)
is
finely
protected
by
the
blood–brain
barrier
(BBB).
Immune
soluble
factors
such
as
cytokines
(CKs)
are
normally
produced
in
CNS,
contributing
to
physiological
immunosurveillance
and
homeostatic
synaptic
scaling.
CKs
peptide,
pleiotropic
molecules
involved
a
broad
range
of
cellular
functions,
with
pivotal
role
resolving
inflammation
promoting
tissue
healing.
However,
pro-inflammatory
can
exert
detrimental
effect
pathological
conditions,
spreading
damage.
In
inflamed
recruit
immune
cells,
stimulate
local
production
other
inflammatory
mediators,
promote
dysfunction.
Our
understanding
neuroinflammation
humans
owes
much
study
multiple
sclerosis
(MS),
most
common
autoimmune
demyelinating
disease,
which
autoreactive
T
cells
migrate
from
periphery
CNS
after
encounter
still
unknown
antigen.
CNS-infiltrating
produce
that
aggravate
demyelination
neurodegeneration.
This
review
aims
recapitulate
state
art
about
healthy
focus
on
recent
advances
bridging
adaptive
neurophysiology.
Proceedings of the National Academy of Sciences,
Journal Year:
2021,
Volume and Issue:
118(50)
Published: Dec. 6, 2021
Significance
Inflammatory
diseases
are
mediated
by
products
such
as
TNF
and
IL-17
produced
T
helper
(Th)
cell
subsets.
Here,
we
identify
a
direct
role
for
in
the
production
of
pathogenic
cells,
particularly
cells
that
produce
(Th17)
interferon-γ
(Th1).
We
found
shapes
inflammatory
response
signaling
via
its
relatively
unstudied
“minor”
receptor,
TNFR2,
skewing
to
become
Th17
enhancing
cytokine
Th1
cells.
Preventing
TNFR2
resulted
reduced
disease
mouse
models
multiple
sclerosis
colitis.
This
work
integrates
importance
with
Th17/Th1
pathogenicity
may
explain
paradox
IL-17–dependent
diseases,
psoriasis
ankylosing
spondylitis,
respond
anti-TNF
monotherapy.
Biology,
Journal Year:
2022,
Volume and Issue:
11(3), P. 372 - 372
Published: Feb. 26, 2022
NF-κB
is
a
central
mediator
of
inflammation,
response
to
DNA
damage
and
oxidative
stress.
As
result
its
role
in
so
many
important
cellular
processes,
dysregulation
has
been
implicated
the
pathology
human
diseases.
activation
causes
inappropriate
inflammatory
responses
diseases
including
rheumatoid
arthritis
(RA)
multiple
sclerosis
(MS).
Thus,
modulation
signaling
being
widely
investigated
as
an
approach
treat
chronic
diseases,
autoimmunity
cancer.
The
emergence
COVID-19
late
2019,
subsequent
pandemic
huge
clinical
burden
patients
with
life-threatening
SARS-CoV-2
pneumonia
led
massive
scramble
repurpose
existing
medicines
lung
inflammation
wide
range
healthcare
systems.
These
efforts
continue
have
proven
be
controversial.
Drug
repurposing
strategies
are
promising
alternative
de
novo
drug
development,
they
minimize
development
timelines
reduce
risk
failure
due
unexpected
side
effects.
Different
experimental
approaches
applied
identify
which
inhibit
that
could
repurposed
anti-inflammatory
drugs.
Molecular Brain,
Journal Year:
2024,
Volume and Issue:
17(1)
Published: Jan. 23, 2024
Abstract
The
central
nervous
system
(CNS)
is
finely
protected
by
the
blood–brain
barrier
(BBB).
Immune
soluble
factors
such
as
cytokines
(CKs)
are
normally
produced
in
CNS,
contributing
to
physiological
immunosurveillance
and
homeostatic
synaptic
scaling.
CKs
peptide,
pleiotropic
molecules
involved
a
broad
range
of
cellular
functions,
with
pivotal
role
resolving
inflammation
promoting
tissue
healing.
However,
pro-inflammatory
can
exert
detrimental
effect
pathological
conditions,
spreading
damage.
In
inflamed
recruit
immune
cells,
stimulate
local
production
other
inflammatory
mediators,
promote
dysfunction.
Our
understanding
neuroinflammation
humans
owes
much
study
multiple
sclerosis
(MS),
most
common
autoimmune
demyelinating
disease,
which
autoreactive
T
cells
migrate
from
periphery
CNS
after
encounter
still
unknown
antigen.
CNS-infiltrating
produce
that
aggravate
demyelination
neurodegeneration.
This
review
aims
recapitulate
state
art
about
healthy
focus
on
recent
advances
bridging
adaptive
neurophysiology.