Pain,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 4, 2025
Abstract
Immune
cells
play
a
critical
role
in
the
transition
from
acute
to
chronic
pain.
However,
of
mast
pain
remains
underinvestigated.
Here,
we
demonstrated
that
resolution
inflammatory
is
markedly
delayed
cell–deficient
mice.
In
response
complete
Freund
adjuvant,
mice
showed
greater
levels
nitric
oxide,
leukocyte
infiltration,
and
altered
cytokine/chemokine
profile
inflamed
skin
both
sexes.
wild-type
mice,
number
cell
cell–derived
chymases,
chymase
1
(CMA1)
protease
4
(MCPT4),
increased
skin.
Inhibiting
enzymatic
activity
Consistently,
local
pharmacological
administration
recombinant
CMA1
MCPT4
promoted
hypersensitivity
attenuated
upregulation
cytokines
chemokines
under
inflammation.
We
identified
CCL9
as
target
MCPT4.
Inhibition
recruitment
CD206
+
myeloid
alleviated
Our
work
reveals
new
chymases
preventing
suggests
therapeutic
avenues
for
treatment
The Journal of Experimental Medicine,
Journal Year:
2019,
Volume and Issue:
217(1)
Published: Oct. 14, 2019
Granulocyte–macrophage
colony-stimulating
factor
(GM-CSF)
has
many
more
functions
than
its
original
in
vitro
identification
as
an
inducer
of
granulocyte
and
macrophage
development
from
progenitor
cells.
Key
features
GM-CSF
biology
need
to
be
defined
better,
such
the
responding
producing
cell
types,
links
with
other
mediators,
prosurvival
versus
activation/differentiation
functions,
when
it
is
relevant
pathology.
Significant
preclinical
data
have
emerged
deletion/depletion
approaches
indicating
that
a
potential
target
inflammatory/autoimmune
conditions.
Clinical
trials
targeting
or
receptor
shown
encouraging
efficacy
safety
profiles,
particularly
rheumatoid
arthritis.
This
review
provides
update
on
above
topics
current
issues/questions
surrounding
biology.
Annual Review of Neuroscience,
Journal Year:
2022,
Volume and Issue:
45(1), P. 339 - 360
Published: April 1, 2022
Interactions
between
the
nervous
and
immune
systems
were
recognized
long
ago,
but
recent
studies
show
that
this
crosstalk
occurs
more
frequently
than
was
previously
appreciated.
Moreover,
technological
advances
have
enabled
identification
of
molecular
mediators
receptors
enable
interaction
these
two
complex
provide
new
insights
on
role
neuroimmune
in
organismal
physiology.
Most
interactions
occur
at
discrete
anatomical
locations
which
neurons
cells
colocalize.
Here,
we
describe
different
branches
peripheral
system
with
various
organs,
including
skin,
intestine,
lung,
adipose
tissue.
We
highlight
how
orchestrates
physiological
processes
such
as
host
defense,
tissue
repair,
metabolism,
thermogenesis.
Unraveling
intricate
relationships
is
invaluable
to
explore
therapeutic
potential
interactions.
Frontiers in Immunology,
Journal Year:
2020,
Volume and Issue:
10
Published: Jan. 28, 2020
A
high
intensity
potentially
tissue
injuring
stimulus
generates
a
homotopic
response
to
escape
the
and
is
associated
with
an
affective
phenotype
considered
represent
pain.
In
face
of
or
nerve
injury,
afferent
encoding
systems
display
robust
changes
in
input-output
function
leading
ongoing
sensation
reported
as
painful
sensitization
nociceptors
such
that
enhanced
pain
state
for
given
somatic
visceral
stimulus.
Our
understanding
mechanisms
underlying
this
nonlinear
processing
nociceptive
stimuli
has
led
our
appreciation
role
played
by
functional
interactions
neural
immune
signaling
phenotypes.
pathological
states,
interact
system
through
actions
variety
soluble
mediators,
including
cytokines.
Cytokines
are
recognized
important
mediators
inflammatory
neuropathic
pain,
supporting
development
persistent
pathologic
can
induce
facilitation
at
all
levels
neuraxis
supraspinal
centers
where
input
evokes
component
state.
We
review
here
several
key
pro-inflammatory
anti-inflammatory
cytokines/chemokines
explore
their
four
neuronal
organization:
1)
peripheral
nociceptor
termini;
2)
dorsal
root
ganglia;
3)
spinal
cord
4)
areas.
Thus,
current
thinking
suggests
cytokines
action
throughout
play
roles
induction
maintenance
facilitated
states
behavior
generated
injury/inflammation
injury.
