Annual Review of Immunology,
Journal Year:
2018,
Volume and Issue:
37(1), P. 173 - 200
Published: Dec. 14, 2018
Malignant
transformation
of
cells
depends
on
accumulation
DNA
damage.
Over
the
past
years
we
have
learned
that
T
cell-based
immune
system
frequently
responds
to
neoantigens
arise
as
a
consequence
this
Furthermore,
recognition
appears
an
important
driver
clinical
activity
both
cell
checkpoint
blockade
and
adoptive
therapy
cancer
immunotherapies.
Here
review
evidence
for
relevance
in
tumor
control
biological
properties
these
antigens.
We
discuss
recent
technological
advances
utilized
identify
neoantigens,
recognize
them,
individual
patients.
Finally,
strategies
can
be
employed
exploit
interventions.
European Journal of Immunology,
Journal Year:
2019,
Volume and Issue:
49(10), P. 1457 - 1973
Published: Oct. 1, 2019
These
guidelines
are
a
consensus
work
of
considerable
number
members
the
immunology
and
flow
cytometry
community.
They
provide
theory
key
practical
aspects
enabling
immunologists
to
avoid
common
errors
that
often
undermine
immunological
data.
Notably,
there
comprehensive
sections
all
major
immune
cell
types
with
helpful
Tables
detailing
phenotypes
in
murine
human
cells.
The
latest
techniques
applications
also
described,
featuring
examples
data
can
be
generated
and,
importantly,
how
analysed.
Furthermore,
tips,
tricks
pitfalls
avoid,
written
peer-reviewed
by
leading
experts
field,
making
this
an
essential
research
companion.
Science,
Journal Year:
2020,
Volume and Issue:
367(6477)
Published: Jan. 31, 2020
Presurgical
immune
checkpoint
blockade
Checkpoint
immunotherapy
using
antibodies
that
inhibit
the
programmed
cell
death
1
(PD-1)
or
cytotoxic
T
lymphocyte–associated
protein
4
(CTLA-4)
pathways
has
resulted
in
unprecedented
clinical
outcomes
for
certain
cancers
such
as
melanoma.
Topalian
et
al.
review
advances
neoadjuvant
(presurgical)
an
important
next
step
enhancing
response
of
early-stage
tumors
to
blockade.
They
highlight
mechanistic
rationale
and
recent
trials
based
on
anti–PD-1
ligand
(anti–PD-L1)
therapy.
Pathological
assessment
criteria
may
provide
early
on-treatment
biomarkers
predict
patient
are
also
discussed.
Science
,
this
issue
p.
eaax0182
Cancer Discovery,
Journal Year:
2019,
Volume and Issue:
9(8), P. 1124 - 1141
Published: June 11, 2019
PD-1
immune
checkpoint
inhibitors
have
produced
encouraging
results
in
patients
with
hepatocellular
carcinoma
(HCC).
However,
what
determines
resistance
to
anti-PD-1
therapies
is
unclear.
We
created
a
novel
genetically
engineered
mouse
model
of
HCC
that
enables
interrogation
how
different
genetic
alterations
affect
surveillance
and
response
immunotherapies.
Expression
exogenous
antigens
MYC;Trp53
-/-
HCCs
led
T
cell-mediated
surveillance,
which
was
accompanied
by
decreased
tumor
formation
increased
survival.
Some
antigen-expressing
escaped
the
system
upregulating
β-catenin
(CTNNB1)
pathway.
Accordingly,
expression
MYC;CTNNB1
had
no
effect,
demonstrating
promoted
escape,
involved
defective
recruitment
dendritic
cells
consequently
impaired
T-cell
activity.
chemokine
CCL5
restored
surveillance.
Finally,
β-catenin-driven
tumors
were
resistant
anti-PD-1.
In
summary,
activation
promotes
escape
could
represent
biomarker
for
patient
exclusion.
SIGNIFICANCE:
Determinants
immunotherapies
are
poorly
understood.
Using
HCC,
we
show
evasion
therapy
potentially
exclusion.See
related
commentary
Berraondo
et
al.,
p.
1003.This
article
highlighted
This
Issue
feature,
983.
Cancer Cell,
Journal Year:
2021,
Volume and Issue:
39(12), P. 1578 - 1593.e8
Published: Oct. 16, 2021
In
triple-negative
breast
cancer
(TNBC),
the
benefit
of
combining
chemotherapy
with
checkpoint
inhibitors
is
still
not
very
clear.
We
utilize
single-cell
RNA-
and
ATAC-sequencing
to
examine
immune
cell
dynamics
in
22
patients
advanced
TNBC
treated
paclitaxel
or
its
combination
anti-PD-L1
atezolizumab.
demonstrate
that
high
levels
baseline
CXCL13+
T
cells
are
linked
proinflammatory
features
macrophages
can
predict
effective
responses
therapy.
responsive
patients,
lymphoid
tissue
inducer
(LTi)
cells,
follicular
B
(Bfoc)
conventional
type
1
dendritic
(cDC1)
concertedly
increase
following
therapy,
but
instead
decrease
after
monotherapy.
Our
data
highlight
importance
therapies
suggest
their
reduction
by
regimen
may
compromise
clinical
outcomes
accompanying
atezolizumab
for
treatment.
