Cells,
Год журнала:
2024,
Номер
13(10), С. 844 - 844
Опубликована: Май 16, 2024
Immune
cell
migration
is
required
for
the
development
of
an
effective
and
robust
immune
response.
This
elegant
process
regulated
by
both
cellular
environmental
factors,
with
variables
such
as
state,
anatomical
location,
disease
state
that
govern
differences
in
patterns.
In
all
cases,
a
major
factor
expression
surface
receptors
their
cognate
ligands.
Rapid
adaptation
to
conditions
partly
depends
on
intrinsic
factors
affect
cell’s
ability
adjust
new
environment.
this
review,
we
discuss
myeloid
lymphoid
cells
outline
key
determinants
migration,
including
molecules
adhesion,
modes
chemotaxis,
specific
chemokine
signaling.
Furthermore,
summarize
tumor-specific
elements
contribute
trafficking
cancer,
while
also
exploring
microenvironment
can
alter
these
dynamics
within
tumor
pro
antitumor
fashion.
Specifically,
highlight
importance
secretome
later
aspects.
review
considers
myriad
impact
trajectory
cancer.
We
aim
immunotherapeutic
targets
be
harnessed
achieve
controlled
tumors.
Cell,
Год журнала:
2024,
Номер
187(10), С. 2485 - 2501.e26
Опубликована: Апрель 22, 2024
Glioma
contains
malignant
cells
in
diverse
states.
Here,
we
combine
spatial
transcriptomics,
proteomics,
and
computational
approaches
to
define
glioma
cellular
states
uncover
their
organization.
We
find
three
prominent
modes
of
First,
gliomas
are
composed
small
local
environments,
each
typically
enriched
with
one
major
state.
Second,
specific
pairs
preferentially
reside
proximity
across
multiple
scales.
This
pairing
is
consistent
tumors.
Third,
these
pairwise
interactions
collectively
a
global
architecture
five
layers.
Hypoxia
appears
drive
the
layers,
as
it
associated
long-range
organization
that
includes
all
cancer
cell
Accordingly,
tumor
regions
distant
from
any
hypoxic/necrotic
foci
tumors
lack
hypoxia
such
low-grade
IDH-mutant
less
organized.
In
summary,
provide
conceptual
framework
for
glioma,
highlighting
tissue
organizer.
Journal of Hematology & Oncology,
Год журнала:
2024,
Номер
17(1)
Опубликована: Май 8, 2024
Abstract
Glioblastoma
(GBM),
the
predominant
and
primary
malignant
intracranial
tumor,
poses
a
formidable
challenge
due
to
its
immunosuppressive
microenvironment,
thereby
confounding
conventional
therapeutic
interventions.
Despite
established
treatment
regimen
comprising
surgical
intervention,
radiotherapy,
temozolomide
administration,
exploration
of
emerging
modalities
such
as
immunotherapy
integration
medicine
engineering
technology
therapy,
efficacy
these
approaches
remains
constrained,
resulting
in
suboptimal
prognostic
outcomes.
In
recent
years,
intensive
scrutiny
inhibitory
milieu
within
GBM
has
underscored
significance
cellular
constituents
microenvironment
their
interactions
with
cells
neurons.
Novel
immune
targeted
therapy
strategies
have
emerged,
offering
promising
avenues
for
advancing
treatment.
One
pivotal
mechanism
orchestrating
immunosuppression
involves
aggregation
myeloid-derived
suppressor
(MDSCs),
glioma-associated
macrophage/microglia
(GAM),
regulatory
T
(Tregs).
Among
these,
MDSCs,
though
constituting
minority
(4–8%)
CD45
+
GBM,
play
central
component
fostering
evasion
propelling
tumor
progression,
angiogenesis,
invasion,
metastasis.
MDSCs
deploy
intricate
mechanisms
that
adapt
dynamic
(TME).
Understanding
interplay
between
provides
compelling
basis
This
review
seeks
elucidate
inherent
explore
existing
targets,
consolidate
insights
into
MDSC
induction
contribution
immunosuppression.
Additionally,
comprehensively
surveys
ongoing
clinical
trials
potential
strategies,
envisioning
future
where
targeting
could
reshape
landscape
GBM.
Through
synergistic
other
modalities,
this
approach
can
establish
multidisciplinary,
multi-target
paradigm,
ultimately
improving
prognosis
quality
life
patients
EBioMedicine,
Год журнала:
2024,
Номер
100, С. 104963 - 104963
Опубликована: Янв. 5, 2024
Glioblastoma
(GBM)
is
one
of
the
most
lethal
central
nervous
systems
(CNS)
tumours
in
adults.
As
supplements
to
standard
care
(SOC),
various
immunotherapies
improve
therapeutic
effect
other
cancers.
Among
them,
tumour
vaccines
can
serve
as
complementary
monotherapy
or
boost
clinical
efficacy
with
immunotherapies,
such
immune
checkpoint
blockade
(ICB)
and
chimeric
antigen
receptor
T
cells
(CAR-T)
therapy.
Previous
studies
GBM
have
suggested
that
few
neoantigens
could
be
targeted
due
low
mutation
burden,
single-peptide
vaccination
had
limited
control
monotherapy.
Combining
diverse
antigens,
including
neoantigens,
tumour-associated
antigens
(TAAs),
pathogen-derived
optimizing
vaccine
design
strategy
may
help
improvement.
In
this
review,
we
discussed
current
platforms,
evaluated
potential
antigenic
targets,
challenges,
perspective
opportunities
for
Abstract
Tumor-associated
macrophages
(TAMs)
are
pivotal
in
cancer
progression,
influencing
tumor
growth,
angiogenesis,
and
immune
evasion.
This
review
explores
the
spatial
temporal
heterogeneity
of
TAMs
within
microenvironment
(TME),
highlighting
their
diverse
subtypes,
origins,
functions.
Advanced
technologies
such
as
single-cell
sequencing
multi-omics
have
elucidated
intricate
interactions
between
other
TME
components,
revealing
mechanisms
behind
recruitment,
polarization,
distribution.
Key
findings
demonstrate
that
support
vascularization,
promote
epithelial-mesenchymal
transition
(EMT),
modulate
extracellular
matrix
(ECM)
remodeling,
etc.,
thereby
enhancing
invasiveness
metastasis.
Understanding
these
complex
dynamics
offers
new
therapeutic
targets
for
disrupting
TAM-mediated
pathways
overcoming
drug
resistance.
underscores
potential
targeting
to
develop
innovative
therapies,
emphasizing
need
further
research
into
characteristics
functional
roles
TME.
Nature Immunology,
Год журнала:
2024,
Номер
25(12), С. 2297 - 2307
Опубликована: Ноя. 8, 2024
Abstract
CD8
+
T
cells
are
critical
mediators
of
antitumor
immunity
but
differentiate
into
a
dysfunctional
state,
known
as
cell
exhaustion,
after
persistent
receptor
stimulation
in
the
tumor
microenvironment
(TME).
Exhausted
(T
ex
)
characterized
by
upregulation
coinhibitory
molecules
and
reduced
polyfunctionality.
TME
experience
an
immunosuppressive
metabolic
environment
via
levels
nutrients
oxygen
buildup
lactic
acid.
Here
we
show
that
terminally
uniquely
upregulate
Slc16a11
,
which
encodes
monocarboxylate
transporter
11
(MCT11).
Conditional
deletion
MCT11
acid
uptake
improved
their
effector
function.
Targeting
with
antibody
lactate
specifically
cells,
which,
when
used
therapeutically
tumor-bearing
mice,
resulted
growth.
These
data
support
model
MCT11,
rendering
them
sensitive
to
present
at
high
TME.
