Trends in cancer,
Journal Year:
2022,
Volume and Issue:
9(3), P. 198 - 211
Published: Dec. 31, 2022
Cytotoxic
T
lymphocytes
(CTLs)
are
antigen-specific
killer
cells
equipped
to
identify
and
eliminate
host
that
have
been
altered
through
infection
or
transformation.
Both
chimeric
antigen-receptor
(CAR)
cell
therapies
immune
checkpoint
blockade
(ICB)
based
on
successful
elimination
of
tumor
by
cytotoxic
effectors.
In
this
opinion
article,
we
outline
cell-intrinsic
mechanisms
which
defend
against
CTLs,
highlighting
pathways
confer
resistance
proposing
opportunities
for
combination
therapies.
We
discuss
how
exogenous
killing
entities
[e.g.,
supramolecular
attack
particles
(SMAPs)]
offer
a
novel
strategy
circumvent
cellular
mechanisms.
Our
article
highlights
the
importance
identifying,
quantifying,
targeting
defense
at
interface
between
CTLs
as
critical
consideration
in
development
immunotherapy
approaches.
Autoimmunity Reviews,
Journal Year:
2024,
Volume and Issue:
23(6), P. 103583 - 103583
Published: June 1, 2024
T
cells
are
key
drivers
of
the
pathogenesis
autoimmune
diseases
by
producing
cytokines,
stimulating
generation
autoantibodies,
and
mediating
tissue
cell
damage.
Distinct
mitochondrial
metabolic
pathways
govern
direction
T-cell
differentiation
function
rely
on
specific
nutrients
enzymes.
Metabolic
substrate
uptake
metabolism
form
foundational
elements
for
activation,
proliferation,
differentiation,
effector
function,
contributing
to
dynamic
interplay
between
immunological
signals
in
coordinating
adaptive
immunity.
Perturbations
availability
enzyme
activity
may
impair
immunosuppressive
fostering
autoreactive
responses
disrupting
immune
homeostasis,
ultimately
disease
pathogenesis.
A
growing
body
studies
has
explored
how
processes
regulate
diverse
subsets
such
as
systemic
lupus
erythematosus
(SLE),
multiple
sclerosis
(MS),
hepatitis
(AIH),
inflammatory
bowel
(IBD),
psoriasis.
This
review
describes
coordination
biology
metabolism,
including
electron
transport
chain
(ETC),
oxidative
phosphorylation,
amino
acid
fatty
one‑carbon
metabolism.
study
elucidated
intricate
crosstalk
programs,
signal
transduction
pathways,
transcription
factors.
summarizes
potential
therapeutic
targets
signaling
diseases,
providing
insights
future
studies.
iScience,
Journal Year:
2024,
Volume and Issue:
27(6), P. 109902 - 109902
Published: May 3, 2024
Highlights•m6A
reader
YTHDF2
was
highly
expressed
in
pro-tumoral
macrophages•YTHDF2
correlates
with
and
immuno-suppressing
signals
of
macrophages•Identification
SPI1
as
key
transcriptional
regulator
YTHDF2-high
macrophage•Ythdf2
associates
phenotype
polarization
macrophages
the
miceSummaryPatients
triple-negative
breast
cancer
(TNBC)
frequently
experience
resistance
to
chemotherapy,
leading
recurrence.
The
approach
optimizing
anti-tumoral
immunological
effect
is
promising
overcoming
such
resistance,
given
heterogeneity
lack
biomarkers
TNBC.
In
this
study,
we
focused
on
YTHDF2,
an
N6-methyladenosine
(m6A)
RNA-reader
protein,
macrophages,
one
most
abundant
intra-tumoral
immune
cells.
Using
single-cell
sequencing
ex
vivo
experiments,
discovered
that
significantly
promotes
closely
associated
down-regulated
antigen-presentation
signaling
other
cells
vitro
deprivation
favors
effect.
Expressions
multiple
transcription
factors,
especially
SPI1,
were
consistently
observed
providing
potential
therapeutic
targets
for
new
strategies.
conclusion,
appears
promote
effects
while
suppressing
activity,
indicating
treatment
targeting
or
its
factors
could
be
a
strategy
chemoresistant
TNBC.Graphical
abstract
Trends in Cell Biology,
Journal Year:
2022,
Volume and Issue:
33(2), P. 138 - 147
Published: June 23, 2022
While
once
regarded
as
ATP
factories,
mitochondria
have
taken
the
spotlight
important
regulators
of
cellular
homeostasis.
The
past
two
decades
witnessed
an
intensifying
interest
in
study
cells
immune
system,
with
many
new
and
unexpected
roles
for
emerging.
Immune
offer
intriguing
insights
appear
to
play
different
at
stages
T
cell
development,
matching
changing
functions
cells.
Here
we
briefly
review
multifaceted
during
differentiation,
focusing
on
CD8+
cytotoxic
lymphocytes
(CTLs)
consider
how
mitochondrial
dysfunction
can
contribute
CTL
exhaustion.
In
addition,
highlight
a
newly
appreciated
role
homeostatic
CTL-mediated
killing
explore
emerging
literature
describing
mechanisms
linking
cytosolic
protein
synthesis.
Trends in cancer,
Journal Year:
2022,
Volume and Issue:
9(3), P. 198 - 211
Published: Dec. 31, 2022
Cytotoxic
T
lymphocytes
(CTLs)
are
antigen-specific
killer
cells
equipped
to
identify
and
eliminate
host
that
have
been
altered
through
infection
or
transformation.
Both
chimeric
antigen-receptor
(CAR)
cell
therapies
immune
checkpoint
blockade
(ICB)
based
on
successful
elimination
of
tumor
by
cytotoxic
effectors.
In
this
opinion
article,
we
outline
cell-intrinsic
mechanisms
which
defend
against
CTLs,
highlighting
pathways
confer
resistance
proposing
opportunities
for
combination
therapies.
We
discuss
how
exogenous
killing
entities
[e.g.,
supramolecular
attack
particles
(SMAPs)]
offer
a
novel
strategy
circumvent
cellular
mechanisms.
Our
article
highlights
the
importance
identifying,
quantifying,
targeting
defense
at
interface
between
CTLs
as
critical
consideration
in
development
immunotherapy
approaches.
