bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 16, 2024
Abstract
Epigenetic
traits
impact
the
antitumor
function
of
CD8
T
cells,
yet
whether
and
how
RNA
methylation
programs
engage
in
cell
immunity
is
poorly
understood.
Here
we
show
that
N
6
-methyladenosine
(m
A)
reader
YTHDF2
highly
expressed
early
effector
or
effector-like
cells
partially
distributed
nucleus.
loss
exacerbates
tumor
progression
confers
unresponsiveness
to
PD-1
blockade
mice
humans.
In
addition
initiating
decay
for
mitochondrial
fitness,
can
orchestrate
chromatin
regulation
promote
polyfunctionality.
YTHDF2-mediatd
preservation
gene
transcription
arises
from
interaction
with
IKZF1/3.
Accordingly,
immunotherapy-induced
efficacy
could
be
largely
restored
YTHDF2-deficient
through
combinational
use
lenalidomide.
Moreover,
m
A
recognition
fundamental
translocation
nucleus
autoregulation
at
level.
Thus,
coordinates
epitranscriptional
transcriptional
networks
potentiate
immunity.
Highlights
expression
distribution
underpin
threshold
bona
fide
response
Canonical
YTHDF2-mRNA
pathway
alleviates
stress
exhaustion
Nuclear
sequesters
IKZF1/3-mediated
repression
safeguard
polyfunctionality
The
tumoricidal
activity
repaired
synergy
anti-PD-1
lenalidomide
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(8), P. 1042 - 1042
Published: Aug. 22, 2024
N6-methyladenosine
(m6A)
represents
the
most
prevalent
and
significant
internal
modification
in
mRNA,
with
its
critical
role
gene
expression
regulation
cell
fate
determination
increasingly
recognized
recent
research.
The
immune
system,
essential
for
defense
against
infections
maintaining
stability
through
interactions
other
bodily
systems,
is
significantly
influenced
by
m6A
modification.
This
acts
as
a
key
post-transcriptional
regulator
of
responses,
though
effects
on
different
cells
vary
across
diseases.
review
delineates
impact
major
system-related
cancers—including
those
respiratory,
digestive,
endocrine,
nervous,
urinary
reproductive,
musculoskeletal
system
malignancies,
well
acute
myeloid
leukemia
autoimmune
We
explore
pathogenic
roles
RNA
modifications
within
tumor
microenvironment
broader
highlighting
how
regulators
interact
pathways
during
disease
progression.
Furthermore,
we
discuss
patterns
these
can
influence
susceptibility
to
immunotherapy,
facilitating
development
diagnostic
prognostic
models
pioneering
new
therapeutic
approaches.
Overall,
this
emphasizes
challenges
prospective
directions
m6A-related
various
systemic
diseases
throughout
body.
Cells,
Journal Year:
2024,
Volume and Issue:
13(18), P. 1526 - 1526
Published: Sept. 11, 2024
Regulatory
T
cells
(Tregs)
play
a
key
role
in
maintaining
immune
homeostasis
and
preventing
autoimmunity
through
their
immunosuppressive
function.
There
have
been
numerous
reports
confirming
that
high
levels
of
Tregs
the
tumor
microenvironment
(TME)
are
associated
with
poor
prognosis,
highlighting
promoting
an
environment.
In
breast
cancer
(BC),
interact
cells,
ultimately
leading
to
suppression
surveillance
progression.
This
review
discusses
dual
cancer,
explores
controversies
therapeutic
potential
targeting
these
cells.
Researchers
investigating
various
strategies
deplete
or
inhibit
Tregs,
such
as
checkpoint
inhibitors,
cytokine
antagonists,
metabolic
inhibition.
However,
heterogeneity
variable
precision
treatments
pose
significant
challenges.
Understanding
functional
diversity
latest
advances
targeted
therapies
is
critical
for
development
effective
therapies.
highlights
approaches
BC
treatment
both
attenuate
Treg-mediated
immunosuppression
tumors
maintain
tolerance,
advocates
precise
combination
therapy
optimize
outcomes.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 16, 2024
Abstract
Epigenetic
traits
impact
the
antitumor
function
of
CD8
T
cells,
yet
whether
and
how
RNA
methylation
programs
engage
in
cell
immunity
is
poorly
understood.
Here
we
show
that
N
6
-methyladenosine
(m
A)
reader
YTHDF2
highly
expressed
early
effector
or
effector-like
cells
partially
distributed
nucleus.
loss
exacerbates
tumor
progression
confers
unresponsiveness
to
PD-1
blockade
mice
humans.
In
addition
initiating
decay
for
mitochondrial
fitness,
can
orchestrate
chromatin
regulation
promote
polyfunctionality.
YTHDF2-mediatd
preservation
gene
transcription
arises
from
interaction
with
IKZF1/3.
Accordingly,
immunotherapy-induced
efficacy
could
be
largely
restored
YTHDF2-deficient
through
combinational
use
lenalidomide.
Moreover,
m
A
recognition
fundamental
translocation
nucleus
autoregulation
at
level.
Thus,
coordinates
epitranscriptional
transcriptional
networks
potentiate
immunity.
Highlights
expression
distribution
underpin
threshold
bona
fide
response
Canonical
YTHDF2-mRNA
pathway
alleviates
stress
exhaustion
Nuclear
sequesters
IKZF1/3-mediated
repression
safeguard
polyfunctionality
The
tumoricidal
activity
repaired
synergy
anti-PD-1
lenalidomide
