Gut Microbes,
Journal Year:
2015,
Volume and Issue:
6(4), P. 234 - 242
Published: July 4, 2015
Polysaccharide
A
(PSA)
derived
from
the
human
commensal
Bacteroides
fragilis
is
a
symbiosis
factor
that
stimulates
immunologic
development
within
mammalian
hosts.
PSA
rebalances
skewed
systemic
T
helper
responses
and
promotes
regulatory
cells
(Tregs).
However,
PSA-mediated
induction
of
Foxp3
in
humans
has
not
been
reported.
In
mice,
PSA-generated
Foxp3+
Tregs
dampen
Th17
activity
thereby
facilitating
bacterial
intestinal
colonization
while
increased
presence
function
these
may
guard
against
pathological
organ-specific
inflammation
We
herein
demonstrate
induces
expression
along
with
CD39
among
naïve
CD4
vitro
promoting
IL-10
secretion.
PSA-activated
dendritic
are
essential
for
mediation
this
response.
When
cultured
isolated
Tregs,
enriched
expression,
enhanced
frequency
CD39+HLA-DR+
cells,
suppressive
as
measured
by
decreased
TNFα
LPS-stimulated
monocytes.
Our
findings
first
to
CD4+Foxp3+
circulating
symbiotic
factor.
Use
treatment
autoimmune
diseases,
particular
multiple
sclerosis
inflammatory
bowel
disease,
represent
new
paradigm
approach
treating
disease.
Cancer Drug Resistance,
Journal Year:
2019,
Volume and Issue:
unknown
Published: Jan. 1, 2019
Cancer
Drug
Resistance
is
an
open
access
journal,
focusing
on
pharmacological
aspects
of
drug
resistance
and
its
reversal,
molecular
mechanisms
classes,
etc.
Both
clinical
experimental
in
cancer
are
included.
Nature Communications,
Journal Year:
2018,
Volume and Issue:
9(1)
Published: July 9, 2018
Abstract
Identifying
tumor
antigen-specific
T
cells
from
cancer
patients
has
important
implications
for
immunotherapy
diagnostics
and
therapeutics.
Here,
we
show
that
CD103
+
CD39
tumor-infiltrating
CD8
(CD8
TIL)
are
enriched
tumor-reactive
both
in
primary
metastatic
tumors.
This
TIL
subset
is
found
across
six
different
malignancies
displays
an
exhausted
tissue-resident
memory
phenotype.
TILs
have
a
distinct
T-cell
receptor
(TCR)
repertoire,
with
clones
expanded
the
but
present
at
low
frequencies
periphery.
also
efficiently
kill
autologous
MHC-class
I-dependent
manner.
Finally,
higher
of
head
neck
associated
better
overall
survival.
Our
data
thus
describe
approach
detecting
will
help
define
mechanisms
existing
treatments,
may
lead
to
future
adoptive
therapies.
OncoImmunology,
Journal Year:
2014,
Volume and Issue:
3(9), P. e955691 - e955691
Published: Sept. 2, 2014
Apoptotic
cells
have
long
been
considered
as
intrinsically
tolerogenic
or
unable
to
elicit
immune
responses
specific
for
dead
cell-associated
antigens.
However,
multiple
stimuli
can
trigger
a
functionally
peculiar
type
of
apoptotic
demise
that
does
not
go
unnoticed
by
the
adaptive
arm
system,
which
we
named
"immunogenic
cell
death"
(ICD).
ICD
is
preceded
accompanied
emission
series
immunostimulatory
damage-associated
molecular
patterns
(DAMPs)
in
precise
spatiotemporal
configuration.
Several
anticancer
agents
successfully
employed
clinic
decades,
including
various
chemotherapeutics
and
radiotherapy,
ICD.
Moreover,
defects
components
underlie
capacity
system
perceive
death
immunogenic
negatively
influence
disease
outcome
among
cancer
patients
treated
with
inducers.
Thus,
has
profound
clinical
therapeutic
implications.
Unfortunately,
gold-standard
approach
detect
relies
on
vaccination
experiments
involving
immunocompetent
murine
models
syngeneic
cells,
an
incompatible
large
screening
campaigns.
Here,
outline
strategies
conceived
surrogate
markers
vitro
screen
chemical
libraries
putative
inducers,
based
high-content,
high-throughput
platform
recently
developed.
Such
allows
detection
DAMPs,
like
surface-exposed
calreticulin,
extracellular
ATP
high
mobility
group
box
1
(HMGB1),
and/or
processes
their
emission,
such
endoplasmic
reticulum
stress,
autophagy
necrotic
plasma
membrane
permeabilization.
We
surmise
this
technology
will
facilitate
development
next-generation
regimens,
kill
malignant
simultaneously
convert
them
into
cancer-specific
vaccine.
Immunological Reviews,
Journal Year:
2017,
Volume and Issue:
276(1), P. 121 - 144
Published: March 1, 2017
Summary
Cancers
are
able
to
grow
by
subverting
immune
suppressive
pathways,
prevent
the
malignant
cells
as
being
recognized
dangerous
or
foreign.
This
mechanism
prevents
cancer
from
eliminated
system
and
allows
disease
progress
a
very
early
stage
lethal
state.
Immunotherapies
newly
developing
interventions
that
modify
patient's
fight
cancer,
either
directly
stimulating
rejection‐type
processes
blocking
pathways.
Extracellular
adenosine
generated
ectonucleotidases
CD
39
73
is
“immune
checkpoint
mediator”
interferes
with
anti‐tumor
responses.
In
this
review,
we
focus
on
ectoenzymes
encompass
aspects
of
biochemistry
these
molecules
well
detailing
distribution
function
cells.
Effects
inhibition
in
preclinical
clinical
studies
discussed.
Finally,
provide
insights
into
potential
application
adenosinergic
other
purinergic‐targeting
therapies
forecast
how
might
develop
combination
anti‐cancer
modalities.
Cell,
Journal Year:
2019,
Volume and Issue:
179(4), P. 964 - 983.e31
Published: Oct. 1, 2019
To
elucidate
the
deregulated
functional
modules
that
drive
clear
cell
renal
carcinoma
(ccRCC),
we
performed
comprehensive
genomic,
epigenomic,
transcriptomic,
proteomic,
and
phosphoproteomic
characterization
of
treatment-naive
ccRCC
paired
normal
adjacent
tissue
samples.
Genomic
analyses
identified
a
distinct
molecular
subgroup
associated
with
genomic
instability.
Integration
proteogenomic
measurements
uniquely
protein
dysregulation
cellular
mechanisms
impacted
by
alterations,
including
oxidative
phosphorylation-related
metabolism,
translation
processes,
phospho-signaling
modules.
assess
degree
immune
infiltration
in
individual
tumors,
microenvironment
signatures
delineated
four
immune-based
subtypes
characterized
pathways.
This
study
reports
large-scale
analysis
to
discern
impact
alterations
provides
evidence
for
rational
treatment
selection
stemming
from
pathobiology.
Pharmacological Reviews,
Journal Year:
2018,
Volume and Issue:
70(2), P. 384 - 411
Published: March 7, 2018
Most
individuals
adjust
their
caffeine
intake
according
to
the
objective
and
subjective
effects
induced
by
methylxanthine.
However,
reach
desired
effects,
quantity
of
consumed
varies
largely
among
individuals.
It
has
been
known
for
decades
that
metabolism,
clearance,
pharmacokinetics
is
affected
many
factors
such
as
age,
sex
hormones,
liver
disease,
obesity,
smoking,
diet.
Caffeine
also
interacts
with
medications.
All
these
will
be
reviewed
in
present
document
discussed
light
most
recent
data
concerning
genetic
variability
affecting
levels
at
pharmacokinetic
pharmacodynamic
both
critically
drive
level
consumption.
The
are
highly
variable
due
a
polymorphism
CYP1A2
isoform
cytochrome
P450,
which
metabolizes
95%
ingested.
Moreover
there
another
critical
enzyme,
N-acetyltransferase
2.
At
level,
several
polymorphisms
main
brain
target
caffeine,
adenosine
A2A
receptor
or
ADORA2.
Genetic
studies,
including
genome-wide
association
identified
loci
involved
consumption
its
consequences
on
sleep,
anxiety,
potentially
neurodegenerative
psychiatric
diseases.
We
start
reaching
better
picture
how
multiplicity
biologic
mechanisms
seems
consumption,
although
much
more
knowledge
still
required
understand
body
functions.
Oncotarget,
Journal Year:
2014,
Volume and Issue:
5(24), P. 12472 - 12508
Published: Dec. 18, 2014
During
the
past
decades,
anticancer
immunotherapy
has
evolved
from
a
promising
therapeutic
option
to
robust
clinical
reality.
Many
immunotherapeutic
regimens
are
now
approved
by
US
Food
and
Drug
Administration
European
Medicines
Agency
for
use
in
cancer
patients,
many
others
being
investigated
as
standalone
interventions
or
combined
with
conventional
treatments
studies.
Immunotherapies
may
be
subdivided
into
"passive"
"active"
based
on
their
ability
engage
host
immune
system
against
cancer.
Since
activity
of
most
passive
immunotherapeutics
(including
tumor-targeting
monoclonal
antibodies)
also
relies
system,
this
classification
does
not
properly
reflect
complexity
drug-host-tumor
interaction.
Alternatively,
can
classified
according
antigen
specificity.
While
some
immunotherapies
specifically
target
one
(or
few)
defined
tumor-associated
antigen(s),
operate
relatively
non-specific
manner
boost
natural
therapy-elicited
responses
unknown
often
broad
Here,
we
propose
critical,
integrated
discuss
relevance
these
approaches.