Science,
Journal Year:
2017,
Volume and Issue:
356(6342), P. 1026 - 1030
Published: June 9, 2017
Tissue
repair
after
injury
is
a
complex,
metabolically
demanding
process.
Depending
on
the
tissue’s
regenerative
capacity
and
quality
of
inflammatory
response,
outcome
generally
imperfect,
with
some
degree
fibrosis,
which
defined
by
aberrant
accumulation
collagenous
connective
tissue.
Inflammatory
cells
multitask
at
wound
site
facilitating
debridement
producing
chemokines,
metabolites,
growth
factors.
If
this
well-orchestrated
response
becomes
dysregulated,
can
become
chronic
or
progressively
fibrotic,
both
outcomes
impairing
tissue
function,
ultimately
lead
to
organ
failure
death.
Here
we
review
current
understanding
role
inflammation
cell
metabolism
in
tissue-regenerative
responses,
highlight
emerging
concepts
that
may
expand
therapeutic
perspectives,
briefly
discuss
where
important
knowledge
gaps
remain.
F1000Prime Reports,
Journal Year:
2014,
Volume and Issue:
6
Published: Feb. 28, 2014
Macrophages
are
endowed
with
a
variety
of
receptors
for
lineage-determining
growth
factors,
T
helper
(Th)
cell
cytokines,
and
B
cell,
host,
microbial
products.
In
tissues,
macrophages
mature
activated
in
dynamic
response
to
combinations
these
stimuli
acquire
specialized
functional
phenotypes.
As
the
lymphocyte
system,
dichotomy
has
been
proposed
macrophage
activation:
classic
vs.
alternative,
also
M1
M2,
respectively.
view
recent
research
about
functions
increasing
number
immune-relevant
ligands,
revision
model
is
needed.
Here,
we
assess
how
cytokines
pathogen
signals
influence
their
phenotypes
evidence
M2
revisit
paradigm
initially
based
on
role
restricted
set
selected
ligands
immune
response.
Journal of Cellular Physiology,
Journal Year:
2018,
Volume and Issue:
233(9), P. 6425 - 6440
Published: Jan. 10, 2018
Macrophages
are
heterogeneous
and
their
phenotype
functions
regulated
by
the
surrounding
micro-environment.
commonly
exist
in
two
distinct
subsets:
1)
Classically
activated
or
M1
macrophages,
which
pro-inflammatory
polarized
lipopolysaccharide
(LPS)
either
alone
association
with
Th1
cytokines
such
as
IFN-γ,
GM-CSF,
produce
interleukin-1β
(IL-1β),
IL-6,
IL-12,
IL-23,
TNF-α;
2)
Alternatively
M2
anti-inflammatory
immunoregulatory
Th2
IL-4
IL-13
IL-10
TGF-β.
macrophages
have
different
transcriptional
profiles.
They
unique
abilities
destroying
pathogens
repair
inflammation-associated
injury.
It
is
known
that
M1/M2
macrophage
balance
polarization
governs
fate
of
an
organ
inflammation
When
infection
severe
enough
to
affect
organ,
first
exhibit
release
TNF-α,
IL-1β,
IL-23
against
stimulus.
But,
if
phase
continues,
it
can
cause
tissue
damage.
Therefore,
secrete
high
amounts
TGF-β
suppress
inflammation,
contribute
repair,
remodeling,
vasculogenesis,
retain
homeostasis.
In
this
review,
we
discuss
basic
biology
including
origin,
differentiation
activation,
distribution,
plasticity
polarization,
migration,
antigen
presentation
capacity,
cytokine
chemokine
production,
metabolism,
involvement
microRNAs
function.
Secondly,
protective
pathogenic
role
subsets
normal
pathological
pregnancy,
anti-microbial
defense,
anti-tumor
immunity,
metabolic
disease
obesity,
asthma
allergy,
atherosclerosis,
fibrosis,
wound
healing,
autoimmunity.
Cellular and Molecular Immunology,
Journal Year:
2020,
Volume and Issue:
17(8), P. 807 - 821
Published: July 1, 2020
Abstract
Immunotherapy
has
revolutionized
cancer
treatment
and
rejuvenated
the
field
of
tumor
immunology.
Several
types
immunotherapy,
including
adoptive
cell
transfer
(ACT)
immune
checkpoint
inhibitors
(ICIs),
have
obtained
durable
clinical
responses,
but
their
efficacies
vary,
only
subsets
patients
can
benefit
from
them.
Immune
infiltrates
in
microenvironment
(TME)
been
shown
to
play
a
key
role
development
will
affect
outcomes
patients.
Comprehensive
profiling
tumor-infiltrating
cells
would
shed
light
on
mechanisms
cancer–immune
evasion,
thus
providing
opportunities
for
novel
therapeutic
strategies.
However,
highly
heterogeneous
dynamic
nature
TME
impedes
precise
dissection
intratumoral
cells.
With
recent
advances
single-cell
technologies
such
as
RNA
sequencing
(scRNA-seq)
mass
cytometry,
systematic
interrogation
is
feasible
provide
insights
into
functional
diversities
In
this
review,
we
outline
progress
particularly
by
focusing
landmark
studies
characterization
tumor-associated
cells,
summarize
phenotypic
connections
with
immunotherapy.
We
believe
review
could
strengthen
our
understanding
facilitate
elucidation
modulation
progression,
guide
immunotherapies
treatment.
Immunity,
Journal Year:
2014,
Volume and Issue:
40(2), P. 274 - 288
Published: Feb. 1, 2014
Highlights•Macrophages
react
with
specific
transcriptional
programming
upon
distinct
signals•Activation
by
TNF,
PGE2,
and
P3C
activates
a
STAT4-associated
program•NFKB1,
JUNB,
CREB1
are
central
transcription
factors
of
macrophage
activation•Inflammatory
signatures
lost
in
alveolar
macrophages
from
COPD
patientsSummaryMacrophage
activation
is
associated
profound
reprogramming.
Although
much
progress
has
been
made
the
understanding
activation,
polarization,
function,
programs
regulating
these
processes
remain
poorly
characterized.
We
stimulated
human
diverse
signals,
acquiring
data
set
299
transcriptomes.
Analysis
this
revealed
spectrum
states
extending
current
M1
versus
M2-polarization
model.
Network
analyses
identified
regulators
all
complemented
related
to
stimulus-specific
programs.
Applying
smokers
patients
chronic
obstructive
pulmonary
disease
(COPD)
an
unexpected
loss
inflammatory
patients.
Finally,
integrating
murine
ImmGen
project
we
propose
refined,
activation-independent
core
signature
for
macrophages.
This
resource
serves
as
framework
future
research
into
regulation
health
disease.Graphical
abstract
