Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Aug. 20, 2021
Immunogenic
cell
death
(ICD)
is
a
form
of
regulated
(RCD)
induced
by
various
stresses
and
produces
antitumor
immunity
via
damage-associated
molecular
patterns
(DAMPs)
release
or
exposure,
mainly
including
high
mobility
group
box
1
(HMGB1),
calreticulin
(CRT),
adenosine
triphosphate
(ATP),
heat
shock
proteins
(HSPs).
Emerging
evidence
has
suggested
that
ionizing
radiation
(IR)
can
induce
ICD,
the
dose,
type,
fractionation
irradiation
influence
induction
ICD.
At
present,
IR-induced
ICD
verified
in
vitro
mice
there
few
clinical
about
it.
To
boost
IR,
some
strategies
have
shown
synergy
with
IR
to
enhance
immune
response,
such
as
hyperthermia,
nanoparticles,
chemotherapy.
In
this
review,
we
focus
on
mechanisms
ICD-promoting
factors
associated
irradiation,
immunogenic
forms
death.
Finally,
summarize
methods
improving
IR.
The EMBO Journal,
Journal Year:
2021,
Volume and Issue:
40(19)
Published: Aug. 30, 2021
Review30
August
2021Open
Access
Autophagy
in
major
human
diseases
Daniel
J
Klionsky
orcid.org/0000-0002-7828-8118
Life
Sciences
Institute,
University
of
Michigan,
Ann
Arbor,
MI,
USA
Search
for
more
papers
by
this
author
Giulia
Petroni
Department
Radiation
Oncology,
Weill
Cornell
Medical
College,
New
York,
NY,
Ravi
K
Amaravadi
Medicine,
Pennsylvania,
Philadelphia,
PA,
Abramson
Cancer
Center,
Eric
H
Baehrecke
Molecular,
Cell
and
Biology,
Massachusetts
School,
Worcester,
MA,
Andrea
Ballabio
orcid.org/0000-0003-1381-4604
Telethon
Institute
Genetics
Pozzuoli,
Italy
Translational
Sciences,
Section
Pediatrics,
Federico
II
University,
Naples,
Molecular
Human
Genetics,
Baylor
College
Jan
Dan
Duncan
Neurological
Research
Texas
Children
Hospital,
Houston,
TX,
Patricia
Boya
orcid.org/0000-0003-3045-951X
Margarita
Salas
Center
Biological
Research,
Spanish
National
Council,
Madrid,
Spain
José
Manuel
Bravo-San
Pedro
Faculty
Physiology,
Complutense
Networked
Biomedical
Neurodegenerative
Diseases
(CIBERNED),
Ken
Cadwell
Kimmel
Biology
Medicine
at
the
Skirball
York
Grossman
School
Microbiology,
Division
Gastroenterology
Hepatology,
Langone
Health,
Francesco
Cecconi
orcid.org/0000-0002-5614-4359
Stress
Survival
Unit,
Autophagy,
Recycling
Disease
(CARD),
Danish
Society
Copenhagen,
Denmark
Pediatric
Onco-Hematology
Gene
Therapy,
IRCCS
Bambino
Gesù
Children's
Rome,
Rome
'Tor
Vergata',
Augustine
M
Choi
Pulmonary
Critical
Care
Joan
Sanford
I.
York-Presbyterian
Mary
E
Nephrology
Hypertension,
Charleen
T
Chu
orcid.org/0000-0002-5052-8271
Pathology,
Pittsburgh
Pittsburgh,
Patrice
Codogno
orcid.org/0000-0002-5492-3180
Institut
Necker-Enfants
Malades,
INSERM
U1151-CNRS
UMR
8253,
Paris,
France
Université
de
Maria
Isabel
Colombo
Laboratorio
Mecanismos
Moleculares
Implicados
en
el
Tráfico
Vesicular
y
la
Autofagia-Instituto
Histología
Embriología
(IHEM)-Universidad
Nacional
Cuyo,
CONICET-
Facultad
Ciencias
Médicas,
Mendoza,
Argentina
Ana
Cuervo
orcid.org/0000-0002-0771-700X
Developmental
Albert
Einstein
Bronx,
Aging
Studies,
Vojo
Deretic
Inflammation
Metabolism
(AIM,
Excellence,
Mexico
Health
Albuquerque,
NM,
Ivan
Dikic
orcid.org/0000-0001-8156-9511
Biochemistry
II,
Goethe
Frankfurt,
Frankfurt
am
Main,
Germany
Buchmann
Zvulun
Elazar
Biomolecular
The
Weizmann
Science,
Rehovot,
Israel
Eeva-Liisa
Eskelinen
Biomedicine,
Turku,
Finland
Gian
Fimia
orcid.org/0000-0003-4438-3325
Sapienza
Epidemiology,
Preclinical
Advanced
Diagnostics,
Infectious
'L.
Spallanzani'
IRCCS,
David
A
Gewirtz
orcid.org/0000-0003-0437-4934
Pharmacology
Toxicology,
Virginia
Commonwealth
Richmond,
VA,
Douglas
R
Green
Immunology,
St.
Jude
Memphis,
TN,
Malene
Hansen
Burnham
Prebys
Discovery
Program
Development,
Aging,
Regeneration,
La
Jolla,
CA,
Marja
Jäättelä
orcid.org/0000-0001-5950-7111
Death
Metabolism,
&
Disease,
Cellular
Terje
Johansen
orcid.org/0000-0003-1451-9578
Group,
Tromsø—The
Arctic
Norway,
Tromsø,
Norway
Gábor
Juhász
Szeged,
Hungary
Anatomy,
Eötvös
Loránd
Budapest,
Vassiliki
Karantza
Merck
Co.,
Inc.,
Kenilworth,
NJ,
Claudine
Kraft
orcid.org/0000-0002-3324-4701
ZBMZ,
Freiburg,
CIBSS
-
Centre
Integrative
Signalling
Guido
Kroemer
orcid.org/0000-0002-9334-4405
Recherche
des
Cordeliers,
Equipe
Labellisée
par
Ligue
Contre
le
Cancer,
Sorbonne
Université,
Inserm
U1138,
Universitaire
France,
Metabolomics
Platforms,
Gustave
Roussy,
Villejuif,
Pôle
Biologie,
Hôpital
Européen
Georges
Pompidou,
AP-HP,
Suzhou
Systems
Chinese
Academy
Suzhou,
China
Karolinska
Women's
Stockholm,
Sweden
Nicholas
Ktistakis
Programme,
Babraham
Cambridge,
UK
Sharad
Kumar
orcid.org/0000-0001-7126-9814
South
Australia,
Adelaide,
SA,
Australia
Carlos
Lopez-Otin
orcid.org/0000-0001-6964-1904
Departamento
Bioquímica
Biología
Medicina,
Instituto
Universitario
Oncología
del
Principado
Asturias
(IUOPA),
Universidad
Oviedo,
Centro
Investigación
Biomédica
Red
Cáncer
(CIBERONC),
Kay
F
Macleod
Ben
May
Gordon
W-338,
Chicago,
IL,
Frank
Madeo
Biosciences,
NAWI
Graz,
Austria
BioTechMed-Graz,
Field
Excellence
BioHealth
–
Jennifer
Martinez
Immunity,
Laboratory,
Environmental
NIH,
Triangle
Park,
NC,
Alicia
Meléndez
Department,
Queens
City
Flushing,
Graduate
PhD
Programs
Noboru
Mizushima
orcid.org/0000-0002-6258-6444
Tokyo,
Japan
Christian
Münz
orcid.org/0000-0001-6419-1940
Viral
Immunobiology,
Experimental
Zurich,
Switzerland
Josef
Penninger
Biotechnology
Austrian
(IMBA),
Vienna
BioCenter
(VBC),
Vienna,
British
Columbia,
Vancouver,
BC,
Canada
Rushika
Perera
orcid.org/0000-0003-2435-2273
California,
San
Francisco,
Helen
Diller
Family
Comprehensive
Mauro
Piacentini
orcid.org/0000-0003-2919-1296
"Tor
Vergata",
Laboratory
Cytology
Russian
Saint
Petersburg,
Russia
Fulvio
Reggiori
orcid.org/0000-0003-2652-2686
Cells
Systems,
Section,
Groningen,
Netherlands
C
Rubinsztein
Cambridge
Dementia
Kevin
Ryan
Beatson
Glasgow,
Junichi
Sadoshima
Cardiovascular
Rutgers
Jersey
Newark,
Laura
Santambrogio
Sandra
Edward
Meyer
Caryl
Englander
Precision
Luca
Scorrano
orcid.org/0000-0002-8515-8928
Istituto
Veneto
di
Medicina
Molecolare,
Padova,
Hans-Uwe
Simon
Pharmacology,
Bern,
Clinical
Immunology
Allergology,
Sechenov
Moscow,
Fundamental
Kazan
Federal
Kazan,
Anna
Katharina
Kennedy
Rheumatology,
NDORMS,
Oxford,
Anne
Simonsen
orcid.org/0000-0003-4711-7057
Basic
Oslo,
Reprogramming,
Oslo
Hospital
Montebello,
Alexandra
Stolz
orcid.org/0000-0002-3340-439X
Nektarios
Tavernarakis
orcid.org/0000-0002-5253-1466
Biotechnology,
Foundation
Technology-Hellas,
Heraklion,
Crete,
Greece
Sharon
Tooze
orcid.org/0000-0002-2182-3116
Francis
Crick
London,
Tamotsu
Yoshimori
orcid.org/0000-0001-9787-3788
Osaka
Suita,
Intracellular
Membrane
Dynamics,
Frontier
Integrated
Science
Division,
Open
Transdisciplinary
Initiatives
(OTRI),
Junying
Yuan
Interdisciplinary
on
Chemistry,
Shanghai
Organic
Shanghai,
Harvard
Boston,
Zhenyu
Yue
Neurology,
Friedman
Brain
Icahn
Mount
Sinai,
Qing
Zhong
orcid.org/0000-0001-6979-955X
Key
Differentiation
Apoptosis
Ministry
Education,
Pathophysiology,
Jiao
Tong
(SJTU-SM),
Lorenzo
Galluzzi
Corresponding
Author
[email
protected]
orcid.org/0000-0003-2257-8500
Dermatology,
Yale
Haven,
CT,
Pietrocola
orcid.org/0000-0002-2930-234X
Biosciences
Nutrition,
Huddinge,
mor
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 Disease,
Journal Year:
2020,
Volume and Issue:
11(11)
Published: Nov. 26, 2020
Abstract
Chemotherapy,
radiation
therapy,
as
well
targeted
anticancer
agents
can
induce
clinically
relevant
tumor-targeting
immune
responses,
which
critically
rely
on
the
antigenicity
of
malignant
cells
and
their
capacity
to
generate
adjuvant
signals.
In
particular,
immunogenic
cell
death
(ICD)
is
accompanied
by
exposure
release
numerous
damage-associated
molecular
patterns
(DAMPs),
altogether
confer
a
robust
adjuvanticity
dying
cancer
cells,
they
favor
recruitment
activation
antigen-presenting
cells.
ICD-associated
DAMPs
include
surface-exposed
calreticulin
(CALR)
secreted
ATP,
annexin
A1
(ANXA1),
type
I
interferon,
high-mobility
group
box
1
(HMGB1).
Additional
hallmarks
ICD
encompass
phosphorylation
eukaryotic
translation
initiation
factor
2
subunit-α
(EIF2S1,
better
known
eIF2α),
autophagy,
global
arrest
in
transcription
translation.
Here,
we
outline
methodological
approaches
for
measuring
markers
vitro
ex
vivo
discovery
next-generation
antineoplastic
agents,
development
personalized
regimens,
identification
optimal
therapeutic
combinations
clinical
management
cancer.
Molecular Cancer,
Journal Year:
2023,
Volume and Issue:
22(1)
Published: Feb. 21, 2023
Abstract
Lung
cancer
is
the
primary
cause
of
mortality
in
United
States
and
around
globe.
Therapeutic
options
for
lung
treatment
include
surgery,
radiation
therapy,
chemotherapy,
targeted
drug
therapy.
Medical
management
often
associated
with
development
resistance
leading
to
relapse.
Immunotherapy
profoundly
altering
approach
owing
its
tolerable
safety
profile,
sustained
therapeutic
response
due
immunological
memory
generation,
effectiveness
across
a
broad
patient
population.
Different
tumor-specific
vaccination
strategies
are
gaining
ground
cancer.
Recent
advances
adoptive
cell
therapy
(CAR
T,
TCR,
TIL),
clinical
trials
on
cancer,
hurdles
discussed
this
review.
patients
(without
targetable
oncogenic
driver
alteration)
reveal
significant
responses
when
treated
programmed
death-1/programmed
death-ligand
1
(PD-1/PD-L1)
checkpoint
blockade
immunotherapies.
Accumulating
evidence
indicates
that
loss
effective
anti-tumor
immunity
tumor
evolution.
vaccines
combined
immune
inhibitors
(ICI)
can
achieve
better
effects.
To
end,
present
article
encompasses
detailed
overview
recent
developments
immunotherapeutic
landscape
targeting
small
(SCLC)
non-small
(NSCLC).
Additionally,
review
also
explores
implication
nanomedicine
immunotherapy
as
well
combinatorial
application
traditional
along
regimens.
Finally,
ongoing
trials,
obstacles,
future
outlook
strategy
highlighted
boost
further
research
field.
Journal of Hematology & Oncology,
Journal Year:
2021,
Volume and Issue:
14(1)
Published: Sept. 27, 2021
Abstract
Immunotherapies
such
as
immune
checkpoint
blockade
(ICB)
and
adoptive
cell
therapy
(ACT)
have
revolutionized
cancer
treatment,
especially
in
patients
whose
disease
was
otherwise
considered
incurable.
However,
primary
secondary
resistance
to
single
agent
immunotherapy
often
results
treatment
failure,
only
a
minority
of
experience
long-term
benefits.
This
review
article
will
discuss
the
relationship
between
response
mechanisms
immunotherapy.
It
also
provide
comprehensive
on
latest
clinical
status
combination
therapies
(e.g.,
with
chemotherapy,
radiation
targeted
therapy),
approved
by
US
Food
Drug
Administration.
an
overview
targeting
cytokines
other
soluble
immunoregulatory
factors,
ACT,
virotherapy,
innate
modifiers
vaccines,
well
that
exploit
alternative
targets
therapeutic
modalities.
Finally,
this
include
stimulating
insights
from
2020
China
Immuno-Oncology
Workshop
co-organized
Chinese
American
Hematologist
Oncologist
Network
(CAHON),
National
Medical
Product
Administration
(NMPA)
Tsinghua
University
School
Medicine.
Journal for ImmunoTherapy of Cancer,
Journal Year:
2021,
Volume and Issue:
9(1), P. e001926 - e001926
Published: Jan. 1, 2021
The
past
decade
has
witnessed
major
breakthroughs
in
cancer
immunotherapy.
This
development
been
largely
motivated
by
cell
evasion
of
immunological
control
and
consequent
tumor
resistance
to
conventional
therapies.
Immunogenic
death
(ICD)
is
considered
one
the
most
promising
ways
achieve
total
elimination.
It
activates
T-cell
adaptive
immune
response
results
formation
long-term
memory.
ICD
can
be
triggered
many
anticancer
treatment
modalities,
including
photodynamic
therapy
(PDT).
In
this
review,
we
first
discuss
role
PDT
based
on
several
classes
photosensitizers,
porphyrins
non-porphyrins,
critically
evaluate
their
potential
induction.
We
emphasize
emerging
trend
induction
combination
with
nanotechnology,
which
represents
third-generation
photosensitizers
involves
targeted
PDT.
However,
also
some
limitations,
reduced
efficiency
hypoxic
microenvironment.
Therefore,
strategies
for
overcoming
limitation,
essential
increasing
efficiency.
final
part,
suggest
areas
future
research
personalized
immunotherapy,
oxygen-boosted
nanoparticles.
conclusion,
insights
from
last
years
increasingly
support
idea
that
a
powerful
strategy
inducing
experimental
therapy.
studies
have
focused
mouse
models,
but
it
necessary
validate
clinical
settings,
will
challenging
area
future.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
24(1), P. 449 - 449
Published: Dec. 27, 2022
Regulated
cell
death
(RCD)
has
a
significant
impact
on
development,
tissue
homeostasis,
and
the
occurrence
of
various
diseases.
Among
different
forms
RCD,
ferroptosis
is
considered
as
type
reactive
oxygen
species
(ROS)-dependent
regulated
necrosis.
ROS
can
react
with
polyunsaturated
fatty
acids
(PUFAs)
lipid
(L)
membrane
via
formation
radical
L•
induce
peroxidation
to
form
L-ROS.
Ferroptosis
triggered
by
an
imbalance
between
hydroperoxide
(LOOH)
detoxification
iron-dependent
L-ROS
accumulation.
Intracellular
iron
accumulation
are
two
central
biochemical
events
leading
ferroptosis.
Organelles,
including
mitochondria
lysosomes
involved
in
regulation
metabolism
redox
In
this
review,
we
will
provide
overview
peroxidation,
well
key
components
ferroptotic
cascade.
The
main
mechanism
that
reduces
ability
glutathione
(GSH).
GSH,
tripeptide
includes
glutamic
acid,
cysteine,
glycine,
acts
antioxidant
substrate
peroxidase
4
(GPX4),
which
then
converted
into
oxidized
(GSSG).
Increasing
expression
GSH
inhibit
We
highlight
role
xc-
GSH-GPX4
pathway
regulate
system
xc-,
composed
subunit
solute
carrier
family
members
(SLC7A11
SLC3A2),
mediates
exchange
cystine
glutamate
across
plasma
synthesize
GSH.
Accumulating
evidence
indicates
requires
autophagy
machinery
for
its
execution.
Ferritinophagy
used
describe
removal
major
storage
protein
ferritin
machinery.
Nuclear
receptor
coactivator
(NCOA4)
cytosolic
bind
subsequent
degradation
ferritinophagy.
During
ferritinophagy,
stored
released
becomes
available
biosynthetic
pathways.
dysfunctional
response
implicated
variety
pathological
conditions.
inducers
or
inhibitors
targeting
redox-
metabolism-related
proteins
signal
transduction
have
been
developed.
simultaneous
detection
intracellular
extracellular
markers
may
help
diagnose
treat
diseases
related
damage.