Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
11
Published: Feb. 5, 2021
We
used
functional
-omics
angles
and
examined
transcriptomic
heterogeneity
in
CD4+Foxp3+
regulatory
T
cells
(Treg)
from
spleen
(s-Treg),
lymph
nodes
(LN-Treg),
intestine
(int-Treg),
visceral
adipose
tissue
(VAT-Treg),
made
significant
findings:
1)
Five
new
shared
Treg
genes
including
NIBAN,
TNFRSF1b,
DUSP4,VAV2,
KLRG1,
68
signatures
are
identified.
Among
27
signaling
pathways
four
Treg,
22
innate
immune
(81.5%);
2)
s-Treg,
LN-Treg,
int-Treg,
VAT-Treg
have
zero,
49,
45,
116
upregulated
pathways,
respectively;
3)
12,
7,
15
out
of
373
CD
markers
identified
as
specific
for
VAT-Treg,
respectively,
which
may
initiate
signaling;
4)
44,
79
increased
cytokines
1176
suggesting
that
much
more
secretory
proteins/cytokines
than
IL-10,
TGF-β,
IL-35;
5)
13
additional
functions
found
by
analyzing
1,706
secretomic
genes;
6)
2,
20,
25,
43
transcription
factors
(TFs)
1,496
TFs
7)
LN-Treg
int-Treg
pyroptosis
regulators
but
apoptosis
regulators;
8)
1,
15,
19,
31
kinases
661
kinome
9)
comparing
with
increase
activated
cluster
(clusters
1-3)
markers;
decrease
resting
4-6)
10)
promote
repair
sharing
secretomes
AHR,
ETV5,
EGR1,
KLF4
stem
cells,
partially
upregulation
all
the
groups
genes.
These
results
suggest
cell-shared
master
make
first
cell
type
using
a
niche
to
maintain
their
Treg-ness
80%
triple
immunosuppression,
repair,
homeostasis
maintenance.
Our
provided
novel
insights
on
roles
therapeutic
targets
cardiovascular
diseases,
chronic
kidney
disease,
autoimmune
transplantation,
cancers.
Frontiers in Immunology,
Journal Year:
2020,
Volume and Issue:
11
Published: Oct. 8, 2020
Severe
COVID-19
patients
show
various
immunological
abnormalities
including
T-cell
reduction
and
cytokine
release
syndrome,
which
can
be
fatal
is
a
major
concern
of
the
pandemic.
However,
it
poorly
understood
how
dysregulation
contribute
to
pathogenesis
severe
COVID-19.
Here
we
single
cell-level
mechanisms
for
in
COVID-19,
demonstrating
new
pathogenetic
activation
differentiation
underlying
By
silico
sorting
CD4+
T-cells
from
cell
RNA-seq
dataset,
found
that
were
highly
activated
showed
unique
pathways
lung
patients.
Notably,
those
expressed
immunoregulatory
receptors
CD25,
whilst
repressing
expression
FOXP3.
Furthermore,
CD25+
hyperactivated
differentiate
into
multiple
helper
lineages,
showing
multifaceted
effector
with
Th1
Th2
characteristics.
Lastly,
CD25-
expressing
produce
protease
Furin,
facilitates
viral
entry
SARS-CoV-2.
Collectively,
are
FOXP3-mediated
negative
feedback
impaired
lung,
may
promote
immunopathology.
Therefore,
our
study
proposes
model
hyperactivation
paralysis
drives
immunopathology
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Oct. 5, 2021
T
regulatory
cells
suppress
a
variety
of
immune
responses
to
self-antigens
and
play
role
in
peripheral
tolerance
maintenance
by
limiting
autoimmune
disorders,
other
pathological
such
as
reactivity
oncoprotein
encoded
antigens.
Forkhead
box
P3
(FOXP3)
expression
is
required
for
Treg
stability
affects
functional
activity.
Mutations
the
master
regulator
FOXP3
related
components
have
been
linked
diseases
humans,
IPEX,
scurfy-like
phenotype
mice.
Several
lines
evidence
indicate
that
use
immunosuppressive
mechanisms
limit
an
response
targeting
effector
cells,
including
secretion
immunoregulatory
cytokines,
granzyme/perforin-mediated
cell
cytolysis,
metabolic
perturbation,
directing
maturation
function
antigen-presenting
(APC)
extracellular
vesicles
development
immunological
tolerance.
In
this
review,
several
highlighted
discussed.
Journal of Translational Medicine,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: March 20, 2024
Abstract
Regulatory
T
cells
(Tregs)
expressing
the
transcription
factor
FoxP3
are
essential
for
maintaining
immunological
balance
and
a
significant
component
of
immunosuppressive
tumor
microenvironment
(TME).
Single-cell
RNA
sequencing
(ScRNA-seq)
technology
has
shown
that
Tregs
exhibit
plasticity
functional
diversity
in
various
tumors
within
TME.
This
results
playing
dual
role
TME,
which
is
not
always
centered
around
supporting
progression
as
typically
believed.
Abundant
data
confirms
anti-tumor
activities
their
correlation
with
enhanced
patient
prognosis
specific
types
malignancies.
In
this
review,
we
summarize
potential
actions
Tregs,
including
suppressing
tumor-promoting
inflammatory
responses
boosting
immunity.
addition,
study
outlines
spatial
temporal
variations
function
to
emphasize
predictive
significance
malignancies
may
change.
It
comprehend
effects
improve
therapy
strategies.
Cellular and Molecular Life Sciences,
Journal Year:
2024,
Volume and Issue:
81(1)
Published: Feb. 29, 2024
Abstract
Advances
in
cancer
immunotherapy
over
the
last
decade
have
led
to
development
of
several
agents
that
affect
immune
checkpoints.
Inhibitory
receptors
expressed
on
T
cells
negatively
regulate
response
include
cytotoxic
T‑lymphocyte
antigen
4
(CTLA4)
and
programmed
cell
death
protein
1
(PD1),
which
been
studied
more
than
similar
receptors.
Inhibition
these
proteins
other
checkpoints
can
stimulate
system
attack
cells,
prevent
tumor
from
escaping
response.
However,
administration
anti-PD1
anti-CTLA4
antibodies
has
associated
with
adverse
inflammatory
responses
autoimmune
diseases.
The
current
review
discussed
role
NF-κB
pathway
as
a
promoter,
how
it
govern
various
More
precise
knowledge
about
communication
between
pathways
could
increase
effectiveness
reduce
effects
checkpoint
inhibitor
therapy.
Graphical
abstract
Annual Review of Pathology Mechanisms of Disease,
Journal Year:
2020,
Volume and Issue:
16(1), P. 123 - 144
Published: Nov. 16, 2020
Helicobacter
pylori
is
the
leading
cause
of
peptic
ulcer
disease.
The
infection
has
been
implicated
in
more
than
75%
duodenal
cases
and
17%
gastric
cases.
H.
classified
as
a
human
carcinogen,
since
it
main
distal
adenocarcinoma
B
cell
mucosa-associated
lymphoid
tissue
lymphoma.
Evidence
also
links
with
extragastric
conditions
including
iron
deficiency
anemia,
idiopathic
thrombocytopenic
purpura,
vitamin
B12
deficiency.
Studies
indicate
that
may
be
protective
against
other
gastrointestinal
tract
(e.g.,
reflux
esophagitis
related
pathologies)
elsewhere
body
asthma).
asymptomatic
vast
majority
cases;
serious
outcomes
occur
only
10-15%
infected
individuals.
Despite
extensive
research
over
past
3
decades,
there
no
effective
vaccine,
circumstances
to
disease
development
remain
unclear.
In
addition,
now
growing
prevalence
antimicrobial
resistance
pylori.
This
review
discusses
these
important
issues.
Seminars in Immunopathology,
Journal Year:
2021,
Volume and Issue:
43(1), P. 45 - 64
Published: Feb. 1, 2021
Abstract
The
thymus
prevents
autoimmune
diseases
through
mechanisms
that
operate
in
the
cortex
and
medulla,
comprising
positive
negative
selection
generation
of
regulatory
T-cells
(Tregs).
Egress
from
perivascular
space
(PVS)
to
blood
is
another
possible
checkpoint,
as
shown
by
some
autoimmune/immunodeficiency
syndromes.
In
polygenic
diseases,
subtle
thymic
dysfunctions
may
compound
genetic,
hormonal
environmental
cues.
Here,
we
cover
(a)
tolerance-inducing
cell
types,
whether
epithelial
or
tuft
cells,
dendritic,
B-
myoid
cells;
(b)
their
failure
relation
anatomic
compartments,
with
special
emphasis
on
human
monogenic
related
pathologies,
if
known;
(c)
polymorphisms
mutations
tolerance-related
genes
an
impact
(e.g.
gene
encoding
thymoproteasome-specific
subunit,
PSMB11
),
promiscuous
expression
AIRE
,
PRKDC
FEZF2
CHD4
Treg
development
SATB1
FOXP3
T-cell
migration
TAGAP
)
egress
MTS1
CORO1A
);
(d)
myasthenia
gravis
prototypic
outcome
inflamed
disordered
neoplastic
‘sick
thymus’.
Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(10)
Published: Oct. 13, 2023
Cancer
immunotherapy
has
transformed
traditional
treatments,
with
immune
checkpoint
blockade
being
particularly
prominent.
However,
minimal
benefit
for
patients
in
most
types
of
cancer
and
is
largely
ineffective
some
cancers
(such
as
pancreatic
glioma).
A
synergistic
anti-tumor
response
may
be
produced
through
the
combined
application
tumor
treatment
methods.
Radiotherapy
(RT)
not
only
kills
cells
but
also
triggers
pro-inflammatory
molecules'
release
cell
infiltration,
which
remodel
microenvironment
(TME).
Therefore,
combination
RT
expected
to
achieve
improved
efficacy.
In
this
review,
we
summarize
effects
on
cellular
components
TME,
including
T
receptor
repertoires,
different
subsets,
metabolism,
tumor-associated
macrophages
other
myeloid
(dendritic
cells,
myeloid-derived
suppressor
neutrophils
eosinophils).
Meanwhile,
non-cellular
such
lactate
extracellular
vesicles
are
elaborated.
addition,
discuss
impact
modalities
immunity
issues
related
clinical
practice
therapy.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: July 22, 2022
Endometriosis
is
defined
as
the
presence
of
endometrial-like
glands
and
stroma
located
outside
uterine
cavity.
This
common,
estrogen
dependent,
inflammatory
condition
affects
up
to
15%
reproductive-aged
women
a
well-recognized
cause
chronic
pelvic
pain
infertility.
Despite
still
unknown
etiology
endometriosis,
much
evidence
suggests
participation
epigenetic
mechanisms
in
disease
etiopathogenesis.
The
main
rationale
based
on
fact
that
heritable
phenotype
changes
do
not
involve
alterations
DNA
sequence
are
common
triggers
for
hormonal,
immunological,
disorders,
which
play
key
role
formation
endometriotic
foci.
Epigenetic
regulating
T-cell
responses,
including
methylation
posttranslational
histone
modifications,
deserve
attention
because
tissue-resident
T
lymphocytes
work
concert
with
organ
structural
cells
generate
appropriate
immune
responses
functionally
shaped
by
organ-specific
environmental
conditions.
Thus,
failure
precisely
regulate
cell
transcription
may
result
compromised
immunological
integrity
an
increased
risk
disorders.
coexistence
endometriosis
autoimmunity
well-known
occurrence.
Recent
research
results
indicate
regulatory
(Treg)
number
highly
active
Tregs
macrophages
have
been
found
peritoneal
fluid
from
endometriosis.
Elimination
function
imbalance
between
helper
Th1
Th2
types
reported
endometria
endometriosis-associated
review
aims
present
state
art
recognition
reprogramming
factor
pathophysiology
context
T-cell-related
autoimmunity.
new
potential
therapeutic
approaches
modulation
and/or
adoptive
transfer
will
also
be
outlined.