Frontiers in Endocrinology,
Journal Year:
2022,
Volume and Issue:
13
Published: June 9, 2022
Nonalcoholic
fatty
liver
disease
(NAFLD)
is
the
dominant
cause
of
worldwide.
steatohepatitis
(NASH),
a
more
aggressive
presentation
NAFLD,
characterized
by
severe
hepatocellular
injury,
inflammation,
and
fibrosis.
Chronic
inflammation
heightened
immune
cell
activity
have
emerged
as
hallmark
features
NASH
key
drivers
fibrosis
through
activation
hepatic
stellate
cells
(HSCs).
Recent
advances
in
our
understanding
molecular
cellular
pathways
highlighted
extensive
crosstalk
between
HSCs
populations
that
strongly
influences
activity.
Here,
we
review
these
findings,
emphasizing
roles
immunity
cell-cell
interactions,
exciting
areas
for
future
investigation.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Aug. 10, 2022
Liver
fibrosis
is
a
common
pathological
feature
of
end
stage
liver
failure,
severe
life-threatening
disease
worldwide.
Nonalcoholic
fatty
(NAFLD),
especially
its
more
form
with
steatohepatitis
(NASH),
results
from
obesity,
type
2
diabetes
and
metabolic
syndrome
becomes
leading
cause
fibrosis.
Genetic
factor,
lipid
overload/toxicity,
oxidative
stress
inflammation
have
all
been
implicated
in
the
development
progression
NASH.
Both
innate
immune
response
adaptive
immunity
contribute
to
NASH-associated
inflammation.
Innate
may
subsequently
via
danger-associated
molecular
patterns.
Increasing
evidence
indicates
that
T
cell-mediated
also
provokes
NASH
cytotoxicity,
cytokines
other
proinflammatory
profibrotic
mediators.
Recently,
single-cell
transcriptome
profiling
has
revealed
populations
CD4
+
cells,
CD8
γδ
TEMs
are
expanded
The
activation
cells
requires
antigen
presentation
professional
antigen-presenting
(APCs),
including
macrophages,
dendritic
B-cells.
However,
since
hepatocytes
express
MHCII
molecules
costimulators,
they
act
as
an
atypical
APC
promote
cell
activation.
Additionally,
phenotypic
switch
contributes
In
this
review,
we
focus
on
particular
discuss
role
different
subsets
Th1,
Th2,
Th17,
Th22,
Treg
NASH-related
Clinical Cancer Research,
Journal Year:
2022,
Volume and Issue:
29(3), P. 513 - 520
Published: Sept. 27, 2022
Abstract
The
last
10
years
have
revolutionized
our
basic
understanding
of
nonalcoholic
fatty
liver
disease
and
consequent
cancer.
It
has
become
clear
that
several
innate
adaptive
immune
cells
play
an
important
role
in
initiating,
maintaining,
or
exacerbating
steatohepatitis
(NASH)—a
been
recently
defined
as
autoaggressive.
Despite
improved
management
aimed
at
reducing
the
progression
fibrosis,
NASH
is
set
to
a
leading
cause
for
hepatocellular
carcinoma
(HCC).
Preliminary
data
from
preclinical
studies
suggest
immunotherapy
efficacy
may
be
reduced
NASH-related
HCC
compared
with
viral
HCC;
however,
conclusive
evidence
supporting
clinical
translation
these
findings
lacking.
Comprehensive
immunologic
phenotyping
mechanisms
linking
carcinogenesis
therapeutic
resistance
key
prevent
cirrhosis,
improve
monitoring
stratification
according
predicted
cancer
risk,
ultimately
increase
survival
patients
NASH-HCC.
In
this
review,
we
summarize
state
art
field
NASH-HCC
focus
on
immunobiology.
We
discuss
underpinning
immunologically
distinct
pro-tumorigenic
entity,
explore
areas
potential
vulnerabilities
NASH-associated
HCC.
Frontiers in Endocrinology,
Journal Year:
2022,
Volume and Issue:
13
Published: June 9, 2022
Nonalcoholic
fatty
liver
disease
(NAFLD)
is
the
dominant
cause
of
worldwide.
steatohepatitis
(NASH),
a
more
aggressive
presentation
NAFLD,
characterized
by
severe
hepatocellular
injury,
inflammation,
and
fibrosis.
Chronic
inflammation
heightened
immune
cell
activity
have
emerged
as
hallmark
features
NASH
key
drivers
fibrosis
through
activation
hepatic
stellate
cells
(HSCs).
Recent
advances
in
our
understanding
molecular
cellular
pathways
highlighted
extensive
crosstalk
between
HSCs
populations
that
strongly
influences
activity.
Here,
we
review
these
findings,
emphasizing
roles
immunity
cell-cell
interactions,
exciting
areas
for
future
investigation.
