Targeting IL-8 and Its Receptors in Prostate Cancer: Inflammation, Stress Response, and Treatment Resistance
Cancers,
Год журнала:
2024,
Номер
16(16), С. 2797 - 2797
Опубликована: Авг. 8, 2024
This
review
delves
into
the
intricate
roles
of
interleukin-8
(IL-8)
and
its
receptors,
CXCR1
CXCR2,
in
prostate
cancer
(PCa),
particularly
castration-resistant
(CRPC)
metastatic
CRPC
(mCRPC).
emphasizes
crucial
role
tumour
microenvironment
(TME)
inflammatory
cytokines
promoting
progression
response
to
cell
targeting
agents.
IL-8,
acting
through
C-X-C
chemokine
receptor
type
1
(CXCR1)
2
(CXCR2),
modulates
multiple
signalling
pathways,
enhancing
angiogenesis,
proliferation,
migration
cells.
highlights
shift
PCa
research
focus
from
solely
cells
non-cancer-cell
components,
including
vascular
endothelial
cells,
extracellular
matrix,
immune
dynamic
interactions
within
TME.
The
immunosuppressive
nature
TME
significantly
influences
resistance
emerging
therapies.
Current
treatment
modalities,
androgen
deprivation
therapy
chemotherapeutics,
encounter
persistent
are
complicated
by
cancer’s
notably
“immune-cold”
nature,
which
limits
system
tumour.
These
challenges
underscore
critical
need
for
novel
approaches
that
both
overcome
enhance
engagement
therapeutic
potential
inhibiting
IL-8
is
explored,
with
studies
showing
enhanced
sensitivity
treatments,
radiation
inhibitors.
Clinical
trials,
such
as
ACE
trial,
demonstrate
efficacy
combining
CXCR2
inhibitors
existing
offering
significant
benefits,
especially
patients
resistant
PCa.
also
addresses
chemokines,
noting
complexity
precision
avoid
side
effects
optimize
outcomes.
Язык: Английский
Anti-CD49d Ab treatment ameliorates age-associated inflammatory response and mitigates CD8+ T-cell cytotoxicity after traumatic brain injury
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Окт. 19, 2024
Abstract
Patients
aged
65
years
and
older
account
for
an
increasing
proportion
of
patients
with
traumatic
brain
injury
(TBI).
Older
TBI
experience
increased
morbidity
mortality
compared
to
their
younger
counterparts.
Our
prior
data
demonstrated
that
by
blocking
α4
integrin,
anti-CD49d
antibody
(aCD49d
Ab)
abrogates
CD8
+
T-cell
infiltration
into
the
injured
brain,
improves
survival,
attenuates
neurocognitive
deficits.
Here,
we
aimed
uncover
how
aCD49d
Ab
treatment
alters
local
cellular
responses
in
mouse
brain.
Consequently,
mice
incur
age-associated
toxic
cytokine
chemokine
long-term
post-TBI.
this
response
along
a
T
helper
(Th)1/Th17
immunological
shift
remediation
overall
cell
cytotoxicity.
Furthermore,
reduces
cells
exhibiting
higher
effector
status,
leading
reduced
clonal
expansion
aged,
but
not
young,
brains
chronic
TBI.
Together,
is
promising
therapeutic
strategy
treating
people.
Язык: Английский