Journal of Hematology & Oncology,
Journal Year:
2020,
Volume and Issue:
13(1)
Published: Aug. 10, 2020
Abstract
In
recent
years,
cancer
immunotherapy
based
on
immune
checkpoint
inhibitors
(ICIs)
has
achieved
considerable
success
in
the
clinic.
However,
ICIs
are
significantly
limited
by
fact
that
only
one
third
of
patients
with
most
types
respond
to
these
agents.
The
induction
cell
death
mechanisms
other
than
apoptosis
gradually
emerged
as
a
new
treatment
strategy
because
tumors
harbor
innate
resistance
apoptosis.
date,
possibility
combining
two
modalities
not
been
discussed
systematically.
Recently,
few
studies
revealed
crosstalk
between
distinct
and
antitumor
immunity.
pyroptosis,
ferroptosis,
necroptosis
combined
showed
synergistically
enhanced
activity,
even
ICI-resistant
tumors.
Immunotherapy-activated
CD8+
T
cells
traditionally
believed
induce
tumor
via
following
main
pathways:
(i)
perforin-granzyme
(ii)
Fas-FasL.
identified
mechanism
which
suppress
growth
inducing
ferroptosis
provoked
review
relationship
system
activation.
Hence,
this
review,
we
summarize
knowledge
reciprocal
interaction
immunity
mechanisms,
particularly
necroptosis,
three
potentially
novel
immunogenic
death.
Because
evidence
is
derived
from
using
animal
models,
also
reviewed
related
bioinformatics
data
available
for
human
tissues
public
databases,
partially
confirmed
presence
interactions
activation
Cell Death and Differentiation,
Journal Year:
2018,
Volume and Issue:
25(3), P. 486 - 541
Published: Jan. 23, 2018
Over
the
past
decade,
Nomenclature
Committee
on
Cell
Death
(NCCD)
has
formulated
guidelines
for
definition
and
interpretation
of
cell
death
from
morphological,
biochemical,
functional
perspectives.
Since
field
continues
to
expand
novel
mechanisms
that
orchestrate
multiple
pathways
are
unveiled,
we
propose
an
updated
classification
subroutines
focusing
mechanistic
essential
(as
opposed
correlative
dispensable)
aspects
process.
As
provide
molecularly
oriented
definitions
terms
including
intrinsic
apoptosis,
extrinsic
mitochondrial
permeability
transition
(MPT)-driven
necrosis,
necroptosis,
ferroptosis,
pyroptosis,
parthanatos,
entotic
death,
NETotic
lysosome-dependent
autophagy-dependent
immunogenic
cellular
senescence,
mitotic
catastrophe,
discuss
utility
neologisms
refer
highly
specialized
instances
these
processes.
The
mission
NCCD
is
a
widely
accepted
nomenclature
in
support
continued
development
field.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(13), P. 3328 - 3328
Published: July 6, 2019
The
NLRP3
inflammasome
is
a
critical
component
of
the
innate
immune
system
that
mediates
caspase-1
activation
and
secretion
proinflammatory
cytokines
IL-1β/IL-18
in
response
to
microbial
infection
cellular
damage.
However,
aberrant
has
been
linked
with
several
inflammatory
disorders,
which
include
cryopyrin-associated
periodic
syndromes,
Alzheimer’s
disease,
diabetes,
atherosclerosis.
activated
by
diverse
stimuli,
multiple
molecular
events,
including
ionic
flux,
mitochondrial
dysfunction,
production
reactive
oxygen
species,
lysosomal
damage
have
shown
trigger
its
activation.
How
responds
those
signaling
events
initiates
assembly
not
fully
understood.
In
this
review,
we
summarize
our
current
understanding
mechanisms
regulation
post-translational
modifications
interacting
partners
NLRP3.
Cell Research,
Journal Year:
2015,
Volume and Issue:
25(12), P. 1285 - 1298
Published: Nov. 27, 2015
Inflammasome
is
an
intracellular
signaling
complex
of
the
innate
immune
system.
Activation
inflammasomes
promotes
secretion
interleukin
1β
(IL-1β)
and
IL-18
triggers
pyroptosis.
Caspase-1
-11
(or
-4/5
in
human)
canonical
non-canonical
inflammasome
pathways,
respectively,
are
crucial
for
inflammasome-mediated
inflammatory
responses.
Here
we
report
that
gasdermin
D
(GSDMD)
another
component
inflammasomes.
We
discovered
presence
GSDMD
protein
nigericin-induced
NLRP3
by
a
quantitative
mass
spectrometry-based
analysis.
Gene
deletion
demonstrated
required
pyroptosis
but
not
proteolytic
maturation
IL-1β
both
It
was
known
substrate
caspase-1
showed
its
cleavage
at
predicted
site
during
activation
this
secretion.
Expression
N-terminal
fragment
can
trigger
cell
death
modification
such
as
tagging
with
Flag
sequence
disrupted
function
GSDMD.
also
found
pro-caspase-1
capable
processing
ASC
essential
to
function.
Further
analyses
LPS
plus
nigericin-
or
Salmonella
typhimurium-treated
macrophage
lines
primary
cells
apoptosis
became
apparent
Gsdmd−/−
cells,
indicating
suppression
The
induction
other
receptors
ASC,
may
partially
contribute
apoptotic
caspases
cells.
These
data
provide
new
insights
into
molecular
mechanisms
reveal
unexpected
interplay
between
