Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Авг. 16, 2023
Amyotrophic
lateral
sclerosis
(ALS)
is
a
chronic,
progressive
neurodegenerative
disease
characterized
by
the
loss
of
motor
neurons.
Dysregulated
peripheral
immunity
has
been
identified
as
hallmark
ALS.
Neutrophils,
front-line
responders
innate
immunity,
contribute
to
host
defense
through
pathogen
clearance.
However,
they
can
concurrently
play
detrimental
role
in
chronic
inflammation.
With
unveiling
novel
functions
neutrophils
diseases,
it
becomes
essential
review
our
current
understanding
and
recognize
gap
knowledge
about
their
Thus,
detailed
comprehension
biological
processes
underlying
neutrophil-induced
pathogenesis
ALS
may
assist
identifying
potential
cell-based
therapeutic
strategies
delay
progression.
Interleukin-17A
(IL-17A)
has
been
implicated
in
the
progression
of
neurodegenerative
diseases
such
as
Alzheimer's
disease
(AD)
and
Parkinson's
(PD).
However,
effect
FDA-approved
Secukinumab
(SEC),
an
IL-17A
inhibitor,
on
PD
remains
unclear.
This
study
aimed
to
investigate
neuroprotective
SEC
its
potential
mechanisms
a
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
(MPTP)-induced
mouse
model
PD.
Male
C57BL/6
J
mice
were
mainly
assigned
three
groups:
Sham,
MPTP,
MPTP
+
SEC.
Motor
coordination
was
assessed
using
climbing
rod
rotarod
tests.
Dopaminergic
neurons
(TH
+)
glial
cells
(Iba-1
,
GFAP
substantia
nigra
evaluated
immunohistochemistry
immunofluorescence.
Flow
cytometry
used
analyze
immune
cell
populations
brain
spleen.
Inflammatory
cytokines
chemokines
quantified
RT-PCR.
treatment
significantly
alleviated
loss
dopaminergic
improved
motor
mice.
It
also
reduced
infiltration
peripheral
cells,
including
CD4
T
NK
monocyte-macrophages
into
brain.
attenuated
activation
decreased
expression
pro-inflammatory
(CCL2,
CXCL9),
which
recruit
These
results
suggest
that
protects
attenuates
neuroinflammation
MPTP-induced
model.
might
be
effective
therapeutic
approach
for
clinical
application
future.
•
reduces
axons
inhibits
Molecular Neurobiology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 10, 2025
Abstract
In
a
healthy
brain,
neuroinflammation,
controlled
by
the
main
intermediary
for
immune
response
microglia
and
astrocytes,
contributes
to
maintain
physiological
functions
such
as
secretion
of
neurotrophic
factors,
removal
cell
tau
amyloid-β
(Aβ)
debris,
local
homeostasis.
When
becomes
chronic,
it
can
become
pathological
fuel
causing
glial
cells
malfunction
not
perform
their
function
clearing
resulting
in
further
damage
neurons.
Multiple
studies
highlight
that
an
intense
crosstalk
is
activated
between
peripheral
blood
white
(PBWCs)
central
nervous
system
(CNS).
Nevertheless,
how
PBWC
be
carriers
biomarkers
CNS
neuropathological
states
still
far
completely
known.
this
work,
we
aimed
observe
content
could
related
moderate-severity
DAT
order
have
early
signals
from
neurodegeneration
brain
initiate.
Protein
analysis
been
performed
Mild
Cognitive
Impairment
(MCI)
patients
respect
those
controls
differently
expressed
proteins
investigated.
Our
data
showed
deregulation
pathways
involved
since
MCI
level
deregulated
considered
markers
onset
progression.
Investigative Ophthalmology & Visual Science,
Год журнала:
2025,
Номер
66(4), С. 15 - 15
Опубликована: Апрель 7, 2025
This
study
aimed
to
explore
the
relationship
between
corneal
nerve
degeneration
and
elevated
dendritic
cells
(DCs)
in
diabetic
keratopathy.
Corneas
from
healthy
mice
were
analyzed
using
single-cell
RNA
sequencing.
Corneal
density
DC
T-cell
infiltration
quantified
through
whole-mount
staining.
Freshly
isolated
mouse
trigeminal
ganglion
(TG)
neurons
co-cultured
with
immature
DCs,
mature
activated
CD8+
T
cells,
CD4+CD25-
cells.
TG
neurite
outgrowth
was
assessed
identify
potential
effector
driving
degeneration.
In
addition,
interferon-gamma
(IFN-γ)
blocking
antibodies
used
evaluate
their
effects
on
mice.
Compared
age-matched
mice,
exhibited
a
significant
reduction
sensitivity,
along
increased
of
CD4+
vitro
co-culture
experiments
revealed
that
rather
than
DCs
significantly
inhibited
outgrowth.
Among
cytokines,
IFN-γ
corneas
impaired
induced
degeneration,
whereas
IL-4
IL-17
had
no
such
effect.
Blocking
alleviated
T-cell-induced
inhibition
but
not
or
contribute
process
partially
mediated
by
IFN-γ.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Авг. 16, 2023
Amyotrophic
lateral
sclerosis
(ALS)
is
a
chronic,
progressive
neurodegenerative
disease
characterized
by
the
loss
of
motor
neurons.
Dysregulated
peripheral
immunity
has
been
identified
as
hallmark
ALS.
Neutrophils,
front-line
responders
innate
immunity,
contribute
to
host
defense
through
pathogen
clearance.
However,
they
can
concurrently
play
detrimental
role
in
chronic
inflammation.
With
unveiling
novel
functions
neutrophils
diseases,
it
becomes
essential
review
our
current
understanding
and
recognize
gap
knowledge
about
their
Thus,
detailed
comprehension
biological
processes
underlying
neutrophil-induced
pathogenesis
ALS
may
assist
identifying
potential
cell-based
therapeutic
strategies
delay
progression.
