Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 12, 2024
Programmed
cell
death
(PCD)
is
an
evolutionarily
conserved
mechanism
of
suicide
that
controlled
by
various
signaling
pathways.
PCD
plays
important
role
in
a
multitude
biological
processes,
such
as
turnover,
development,
tissue
homeostasis
and
immunity.
Some
forms
PCD,
including
apoptosis,
autophagy-dependent
death,
pyroptosis,
ferroptosis
necroptosis,
contribute
to
carcinogenesis
cancer
thus
have
attracted
increasing
attention
the
field
oncology.
Recently,
research-based
evidence
has
demonstrated
acts
critical
modulator
tumor
can
affect
function
innate
adaptive
immune
cells,
which
leads
distinct
immunological
consequences,
priming
tumor-specific
T
immunosuppression
evasion.
Targeting
alone
or
combination
with
conventional
immunotherapy
may
provide
new
options
enhance
clinical
efficacy
anticancer
therapeutics.
In
this
review,
we
introduce
characteristics
mechanisms
ubiquitous
pathways
(e.g.,
pyroptosis
ferroptosis)
explore
complex
interaction
between
these
immunity
based
on
currently
available
evidence.
We
also
discuss
therapeutic
potential
PCD-based
approaches
outlining
trials
targeting
treatment.
Elucidating
immune-related
effects
pathogenesis
will
likely
improved
understanding
oncoimmunology
allow
be
exploited
for
Abstract
Nanomedicine‐assisted
sonodynamic
therapy
(SDT)
has
emerged
as
one
of
the
most
promising
cancer
therapies
due
to
its
unique
advantages
high
penetration,
non‐radiation,
and
excellent
oxidative
stress
effect,
but
always
suffered
from
self‐protection
mechanism
apoptosis
resistance
characteristics
evolutionarily
mutated
cells.
Regulated
cell
death
(RCD)
received
increasing
attention
in
precision
treatments
because
significant
role
synergistically
sensitizing
reversing
immunosuppressive
microenvironment
during
SDT
nanomedicine‐triggered
immunogenic
death.
Herein,
paradigmatic
research
RCD‐augmented
tumor
immunotherapeutics
are
typically
introduced,
such
autophagy
blockade,
ferroptosis
targeting,
pyroptosis
induction,
necroptosis
initiation,
cuproptosis
actuation,
PANoptosis
trigger,
coordinated
anti‐tumor
mechanisms
discussed
detail.
Multiple
analysis
focusing
on
currently
unsolved
problems
future
development
prospects
RCD‐based
nano‐oncology
medicine
also
prospected
further
strengthen
expand
scope
therapeutic
applications.
Emerging Microbes & Infections,
Год журнала:
2024,
Номер
13(1)
Опубликована: Март 19, 2024
African
swine
fever
(ASF)
is
a
highly
contagious,
often
fatal
viral
disease
caused
by
virus
(ASFV)
that
imposes
substantial
economic
burden
on
the
global
pig
industry
each
year.
When
screening
for
regulation
of
replication
genes
in
left
variable
region
ASFV
genome,
we
observed
notable
reduction
following
deletion
MGF300-4L
gene.
However,
role
infection
remains
unexplored.
In
this
study,
found
could
effectively
inhibit
production
proinflammatory
cytokines
IL-1β
and
TNF-α,
which
are
regulated
NF-κB
signaling
pathway.
Mechanistically,
demonstrated
interacts
with
IKKβ
promotes
its
lysosomal
degradation
via
chaperone-mediated
autophagy.
Meanwhile,
interaction
between
IκBα
competitively
inhibits
binding
E3
ligase
β-TrCP
to
IκBα,
thereby
inhibiting
ubiquitination-dependent
IκBα.
Remarkably,
despite
encoding
other
inhibitors
NF-κB,
gene-deleted
(Del4L)
showed
reduced
virulence
pigs,
indicating
plays
critical
pathogenicity.
Importantly,
attenuation
Del4L
was
associated
significant
increase
TNF-α
during
early
stages
pigs.
Our
findings
provide
insights
into
functions
pathogenicity,
suggesting
be
promising
target
developing
novel
strategies
live
attenuated
vaccines
against
ASF.
Autophagy,
Год журнала:
2024,
Номер
20(12), С. 2655 - 2676
Опубликована: Июль 25, 2024
Spautin-1
is
a
well-known
macroautophagy/autophagy
inhibitor
via
suppressing
the
deubiquitinases
USP10
and
USP13
promoting
degradation
of
PIK3C3/VPS34-BECN1
complex,
while
its
effect
on
selective
autophagy
remains
poorly
understood.
Mitophagy
form
for
removal
damaged
superfluous
mitochondria
autophagy-lysosome
pathway.
Here,
we
report
surprising
discovery
that,
spautin-1
as
an
effective
inhibitor,
it
promotes
PINK1-PRKN-dependent
mitophagy
induced
by
mitochondrial
damage
agents.
Mechanistically,
facilitates
stabilization
activation
full-length
PINK1
at
outer
membrane
(OMM)
binding
to
components
TOMM
complex
(TOMM70
TOMM20),
leading
disruption
import
prevention
PARL-mediated
cleavage.
Moreover,
induces
neuronal
in
Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 12, 2024
Programmed
cell
death
(PCD)
is
an
evolutionarily
conserved
mechanism
of
suicide
that
controlled
by
various
signaling
pathways.
PCD
plays
important
role
in
a
multitude
biological
processes,
such
as
turnover,
development,
tissue
homeostasis
and
immunity.
Some
forms
PCD,
including
apoptosis,
autophagy-dependent
death,
pyroptosis,
ferroptosis
necroptosis,
contribute
to
carcinogenesis
cancer
thus
have
attracted
increasing
attention
the
field
oncology.
Recently,
research-based
evidence
has
demonstrated
acts
critical
modulator
tumor
can
affect
function
innate
adaptive
immune
cells,
which
leads
distinct
immunological
consequences,
priming
tumor-specific
T
immunosuppression
evasion.
Targeting
alone
or
combination
with
conventional
immunotherapy
may
provide
new
options
enhance
clinical
efficacy
anticancer
therapeutics.
In
this
review,
we
introduce
characteristics
mechanisms
ubiquitous
pathways
(e.g.,
pyroptosis
ferroptosis)
explore
complex
interaction
between
these
immunity
based
on
currently
available
evidence.
We
also
discuss
therapeutic
potential
PCD-based
approaches
outlining
trials
targeting
treatment.
Elucidating
immune-related
effects
pathogenesis
will
likely
improved
understanding
oncoimmunology
allow
be
exploited
for
