Annual Review of Immunology,
Journal Year:
2015,
Volume and Issue:
33(1), P. 643 - 675
Published: March 21, 2015
Macrophages
are
myeloid
immune
cells
that
strategically
positioned
throughout
the
body
tissues,
where
they
ingest
and
degrade
dead
cells,
debris,
foreign
material
orchestrate
inflammatory
processes.
Here
we
review
two
major
recent
paradigm
shifts
in
our
understanding
of
tissue
macrophage
biology.
The
first
is
realization
most
tissue-resident
macrophages
established
prenatally
maintained
through
adulthood
by
longevity
self-renewal.
Their
generation
maintenance
thus
independent
from
ongoing
hematopoiesis,
although
can
be
complemented
adult
monocyte-derived
macrophages.
Second,
aside
being
sentinels,
form
integral
components
their
host
tissue.
This
entails
specialization
response
to
local
environmental
cues
contribute
development
specific
function
residence.
Factors
govern
emerging.
Moreover,
reflected
discrete
gene
expression
profiles
macrophages,
as
well
epigenetic
signatures
reporting
actual
potential
enhancer
usage.
Annual Review of Physiology,
Journal Year:
2016,
Volume and Issue:
79(1), P. 541 - 566
Published: Nov. 4, 2016
Macrophage
polarization
refers
to
how
macrophages
have
been
activated
at
a
given
point
in
space
and
time.
Polarization
is
not
fixed,
as
are
sufficiently
plastic
integrate
multiple
signals,
such
those
from
microbes,
damaged
tissues,
the
normal
tissue
environment.
Three
broad
pathways
control
polarization:
epigenetic
cell
survival
that
prolong
or
shorten
macrophage
development
viability,
microenvironment,
extrinsic
factors,
microbial
products
cytokines
released
inflammation.
A
plethora
of
advances
provided
framework
for
rationally
purifying,
describing,
manipulating
polarization.
Here,
I
assess
current
state
knowledge
about
enumerate
major
questions
regulate
physiology
tissues.
Physiological Reviews,
Journal Year:
2018,
Volume and Issue:
98(4), P. 2133 - 2223
Published: Aug. 1, 2018
The
1921
discovery
of
insulin
was
a
Big
Bang
from
which
vast
and
expanding
universe
research
into
action
resistance
has
issued.
In
the
intervening
century,
some
discoveries
have
matured,
coalescing
solid
fertile
ground
for
clinical
application;
others
remain
incompletely
investigated
scientifically
controversial.
Here,
we
attempt
to
synthesize
this
work
guide
further
mechanistic
investigation
inform
development
novel
therapies
type
2
diabetes
(T2D).
rational
such
necessitates
detailed
knowledge
one
key
pathophysiological
processes
involved
in
T2D:
resistance.
Understanding
resistance,
turn,
requires
normal
action.
review,
both
physiology
pathophysiology
are
described,
focusing
on
three
target
tissues:
skeletal
muscle,
liver,
white
adipose
tissue.
We
aim
develop
an
integrated
physiological
perspective,
placing
intricate
signaling
effectors
that
carry
out
cell-autonomous
response
context
tissue-specific
functions
generate
coordinated
organismal
response.
First,
section
II,
effects
direct,
tissue
reviewed,
beginning
at
receptor
working
downstream.
Section
III
considers
critical
underappreciated
role
crosstalk
whole
body
action,
especially
essential
interaction
between
lipolysis
hepatic
gluconeogenesis.
is
then
described
IV.
Special
attention
given
pathways
become
resistant
setting
chronic
overnutrition,
alternative
explanation
phenomenon
‟selective
resistanceˮ
presented.
Sections
V,
VI,
VII
critically
examine
evidence
against
several
putative
mediators
V
reviews
linking
bioactive
lipids
diacylglycerol,
ceramide,
acylcarnitine
resistance;
VI
impact
nutrient
stresses
endoplasmic
reticulum
mitochondria
discusses
non-cell
autonomous
factors
proposed
induce
including
inflammatory
mediators,
branched-chain
amino
acids,
adipokines,
hepatokines.
Finally,
VIII,
propose
model
links
these
final
common
metabolite-driven
gluconeogenesis
ectopic
lipid
accumulation.
Genes & Development,
Journal Year:
2018,
Volume and Issue:
32(19-20), P. 1267 - 1284
Published: Oct. 1, 2018
The
presence
of
inflammatory
immune
cells
in
human
tumors
raises
a
fundamental
question
oncology:
How
do
cancer
avoid
the
destruction
by
attack?
In
principle,
tumor
development
can
be
controlled
cytotoxic
innate
and
adaptive
cells;
however,
as
develops
from
neoplastic
tissue
to
clinically
detectable
tumors,
evolve
different
mechanisms
that
mimic
peripheral
tolerance
order
tumoricidal
attack.
Here,
we
provide
an
update
recent
accomplishments,
unifying
concepts,
future
challenges
study
tumor-associated
cells,
with
emphasis
on
metastatic
carcinomas.
Annual Review of Pathology Mechanisms of Disease,
Journal Year:
2019,
Volume and Issue:
15(1), P. 123 - 147
Published: Sept. 18, 2019
Macrophages
are
a
diverse
set
of
cells
present
in
all
body
compartments.
This
diversity
is
imprinted
by
their
ontogenetic
origin
(embryonal
versus
adult
bone
marrow-derived
cells);
the
organ
context;
activation
or
deactivation
various
signals
contexts
microbial
invasion,
tissue
damage,
and
metabolic
derangement;
polarization
adaptive
T
cell
responses.
Classic
responses
macrophages
include
tolerance,
priming,
wide
spectrum
states,
including
M1,
M2,
M2-like.
Moreover,
can
retain
long-term
imprinting
encounters
(trained
innate
immunity).
Single-cell
analysis
mononuclear
phagocytes
health
disease
has
added
new
dimension
to
our
understanding
macrophage
differentiation
activation.
Epigenetic
landscapes,
transcription
factors,
microRNA
networks
underlie
adaptability
different
environmental
cues.
Macrophage
plasticity,
an
essential
component
chronic
inflammation,
its
involvement
human
diseases,
most
notably
cancer,
discussed
here
as
paradigm.
