Abstract
Objectives
The
aim
of
this
study
was
to
characterise
the
dynamic
immune
profile
paediatric
burn
patients
for
up
18
months
post‐burn.
Methods
Flow
cytometry
used
measure
25
cell
markers,
chemokines
and
cytokines
which
reflected
both
pro‐inflammatory
anti‐inflammatory
profiles.
Peripheral
blood
mononuclear
cells
from
6
who
had
returned
repeated
scar
treatments
>
4
timepoints
within
12
post‐burn
were
compared
four
age‐matched
healthy
controls.
Results
While
overall
proportions
T
cells,
NK
macrophages
remained
relatively
constant,
over
time
percentages
these
differentiated
into
effector
proinflammatory
phenotypes
including
Th17
activated
γδ
cells.
Circulating
increased
their
expression
mediators
throughout
recovery,
with
a
3–6
fold
increase
IL‐17
at
1–3
weeks,
NFκβ
9–18
T‐regulatory
plasticity
also
observed,
Treg
phenotype
changed
systemically
reduced
skin‐homing
T‐regs
(CCR4
+
)
inflammatory
(CCR6
1‐month
post‐burn,
double‐positive
types
CCR6
elevated
in
circulation
Furthermore,
Tregs
observed
proportionally
express
less
IL‐10
but
TNF‐α
months.
Conclusion
Overall,
results
indicate
circulating
do
not
or
decrease
instead
they
become
highly
specialised,
skin‐homing.
In
patient
population,
changes
persisted
least
‘immune
distraction’
may
limit
ability
prioritise
other
threats
such
as
respiratory
infections.
Recent
studies
reveal
that
lateral
mitochondrial
transfer,
the
movement
of
mitochondria
from
one
cell
to
another,
can
affect
cellular
and
tissue
homeostasis.
Most
what
we
know
about
transfer
stems
bulk
have
led
paradigm
functional
transferred
restore
bioenergetics
revitalize
functions
recipient
cells
with
damaged
or
non-functional
networks.
However,
show
also
occurs
between
functioning
endogenous
networks,
but
mechanisms
underlying
how
promote
such
sustained
behavioral
reprogramming
remain
unclear.
We
report
unexpectedly,
macrophage
are
dysfunctional
accumulate
reactive
oxygen
species
in
cancer
cells.
further
discovered
accumulation
activates
ERK
signaling,
promoting
proliferation.
Pro-tumorigenic
macrophages
exhibit
fragmented
leading
higher
rates
Finally,
observe
promotes
tumor
proliferation
vivo.
Collectively
these
results
indicate
activate
downstream
signaling
pathways
a
ROS-dependent
manner
cells,
provide
model
be
mediated
by
relatively
small
amount
vitro
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
163, P. 114824 - 114824
Published: May 2, 2023
CD8+
T
cells
are
the
front-line
defensive
against
cancer.
Reduced
infiltration
and
effector
function
of
occurs
in
cancer
is
contributed
to
defective
immunity
immunotherapy
resistance.
Exclusion
exhaustion
two
key
factors
associated
with
reduced
durability
immune
checkpoint
inhibitor
(ICI)
therapy.
Initially
activated
upon
exposure
chronic
antigen
stimulation
or
immunosuppressive
tumor
microenvironment
(TME)
acquire
a
hyporesponsive
state
that
progressively
lose
their
function.
Thus,
strategy
look
for
cell
Targeting
such
can
define
promising
supplementary
approach
patients
receiving
anti-programmed
death-1
receptor
(PD-1)/anti-programmed
death-ligand
1
(PD-L1)
Recently,
bispecific
antibodies
developed
PD-(L)1
dominant
factor
within
TME,
representing
higher
safety
profile
exerting
more
desired
outcomes.
The
focus
this
review
discuss
about
promoters
deficient
addressing
ICI
PubMed,
Journal Year:
2024,
Volume and Issue:
27(4), P. 245 - 256
Published: April 20, 2024
Tumor
microenvironment
(TME)
is
one
of
the
important
factors
in
tumorigenesis
and
progression,
which
tumor-associated
macrophages
(TAMs)
play
an
role
non-small
cell
lung
cancer
(NSCLC)
progression.
However,
mechanism
TAMs
NSCLC
progression
remains
unclear,
so
this
study
aimed
to
investigate
find
potential
therapeutic
targets.
