bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: July 19, 2023
SUMMARY
Preterm
birth
(PTB),
often
preceded
by
preterm
labor,
is
a
major
cause
of
neonatal
morbidity
and
mortality
worldwide.
Most
PTB
cases
involve
intra-amniotic
inflammation
without
detectable
microorganisms,
termed
in
utero
sterile
inflammation,
for
which
there
no
established
treatment.
Here,
we
propose
homeostatic
macrophages
to
prevent
adverse
outcomes
caused
inflammation.
Single-cell
atlases
the
maternal-fetal
interface
revealed
that
maternal
are
reduced
with
human
labor.
M2
macrophage
treatment
prevented
mice
Specifically,
halted
premature
labor
suppressing
inflammatory
responses
amniotic
cavity,
including
inflammasome
activation,
mitigated
placental
offspring
lung
Moreover,
restored
gut
homeostasis
enhanced
resistance
systemic
bacterial
infection.
Our
findings
show
promising
strategy
mitigate
improve
from
Inflammation Research,
Journal Year:
2025,
Volume and Issue:
74(1)
Published: March 4, 2025
Parturition
is
similar
to
an
inflammatory
response
in
which
resident
and
infiltrating
immune
cells
release
cytokines
chemokines
into
the
maternal-fetal
interface,
promoting
expulsion
of
fetus
from
mother.
The
untimely
activation
these
pathways
can
result
preterm
labor.
interface
composed
mainly
decidual
tissue
placental
villous
space.
objective
this
review
examine
role
mechanisms
during
parturition
birth.
A
deeper
understanding
at
could
provide
significant
insight
birth
pathogenesis.
We
searched
major
databases
(including
PubMed,
Web
Science,
Google
Scholar
etc.)
for
literature
encompassing
cells,
up
July
2024
combined
with
studies
found
reference
lists
included
studies.
Decidual
neutrophils
mediators
that
facilitate
parturition.
M1/M2
ratio
macrophages
increases
among
population.
Mast
may
cause
uterine
contractions.
In
birth,
there
increase
CD56dimCD16+
natural
killer
immature
dendritic
cells.
Th1/Th2
Th17/Treg
leads
Women
had
a
higher
proportion
B
ILC2
help
protect
steady-state
environment
interface.
invariant
NKT
plays
important
inflammation-induced
These
communicate
each
other.
development
sequencing
technology
enables
more
in-depth
study
dynamic
balance
microenvironment
crucial
maintaining
human
pregnancy
initiation
delivery.
deep
mechanism
dysfunction
pathogenesis
American Journal of Reproductive Immunology,
Journal Year:
2025,
Volume and Issue:
93(2)
Published: Feb. 1, 2025
ABSTRACT
Recurrent
pregnancy
loss
(RPL)
is
characterized
by
the
occurrence
of
two
or
more
consecutive
losses.
Approximately
half
these
cases
lack
a
clear
etiology
and
are
termed
unexplained
recurrent
(URPL).
Maternal–fetal
immune
dysfunction
thought
to
be
involved
in
causing
URPL.
Increased
human
leukocyte
antigen
compatibility,
susceptibility
genes,
blocking
antibodies,
cells
can
all
disrupt
tolerance
environment
maternal–fetal
interface.
To
correct
imbalances,
some
immunotherapies
were
recently
tried
used
for
patients
with
This
review
summarizes
characteristics
mechanisms
microenvironment
at
interface
URPL
patients,
present
serve
as
reference
future
research.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 7, 2024
B
cells
constitute
a
diverse
and
adaptable
immune
cell
population
with
functions
that
can
vary
according
to
the
environment
circumstances.
The
involvement
of
in
pregnancy,
as
well
associated
molecular
pathways,
has
yet
be
investigated.
This
review
consolidates
current
knowledge
on
activities
regulation
during
particular
focus
roles
various
subsets
effects
cell-derived
factors
pregnancy
outcomes.
Moreover,
examines
significance
cell-associated
autoantibodies,
cytokines,
signaling
pathways
relation
complications
such
loss,
preeclampsia,
preterm
birth.
European Journal of Obstetrics & Gynecology and Reproductive Biology X,
Journal Year:
2025,
Volume and Issue:
25, P. 100371 - 100371
Published: Feb. 6, 2025
Precisely
timed
immune
adaptations,
observed
in
the
maternal
circulation,
underpin
notion
of
an
clock
human
pregnancy
that
supports
its
successful
progression
and
completion
at
delivery.
This
is
divided
into
three
immunological
phases,
with
first
phase
starting
time
conception
implantation,
shifting
second
homeostasis
tolerance
throughout
pregnancy,
culminating
last
labor
parturition.
Disruptions
this
are
reported
complications
such
as
spontaneous
preterm
birth.
However,
our
understanding
preceding
birth
remains
scattered.
In
review,
we
describe
chronology
cell
adaptations
during
healthy
pregnancies
highlight
disruption
With
a
focus
on
single-cell
cytometric,
proteomic
transcriptomic
approaches,
review
recent
studies
term
discuss
need
for
future
prospective
aimed
tracking
longitudinally
multi-omic
scale.
Such
will
be
critical
determining
whether
progress
accelerated
pace
or
follow
preterm-intrinsic
pattern
when
compared
to
those
delivered
term.
Science Translational Medicine,
Journal Year:
2025,
Volume and Issue:
17(789)
Published: March 12, 2025
Congenital
cytomegalovirus
(cCMV)
is
the
leading
infectious
cause
of
neonatal
neurological
impairment
worldwide,
but
viral
factors
enabling
vertical
spread
across
placenta
remain
undetermined.
The
pentameric
complex
(PC),
composed
subunits
gH/gL/UL128/UL130/UL131A,
has
been
demonstrated
to
be
important
for
entry
into
nonfibroblast
cells
in
vitro.
These
findings
link
PC
broad
cell
tropism
and
virus
dissemination
vivo,
denoting
all
as
potential
targets
intervention
strategies
vaccine
development.
To
determine
relevance
congenital
transmission
a
translational
nonhuman
primate
model,
we
engineered
rhesus
CMV
(RhCMV)
mutant
lacking
orthologs
UL128
UL130,
which
diminished
infection
epithelial
However,
intravenous
inoculation
either
CD4
+
T
cell–depleted
or
immunocompetent
RhCMV-seronegative
pregnant
macaques
(RMs)
early
second
trimester
with
PC-deficient
resulted
maternal
RhCMV
peak
plasma
viremia
similar
inoculations
PC-intact
RhCMV,
although
shedding
saliva
urine
was
limited.
Infections
induced
IgG
responses
that
neutralized
tissue
culture.
were
reduced,
not
absent,
from
animals
infected
virus,
also
against
gH.
Moreover,
confirmed
multiple
by
detecting
DNA
amniotic
fluid,
indicating
transplacental
RMs
contingent
on
PC.
American Journal of Obstetrics and Gynecology,
Journal Year:
2025,
Volume and Issue:
232(4), P. S160 - S175.e7
Published: April 1, 2025
COVID-19
in
pregnancy
is
associated
with
placental
immune
activation,
inflammation,
and
vascular
malperfusion,
but
its
impact
on
syncytiotrophoblast
biology
function
unclear.
This
study
aimed
to
determine
the
effects
of
maternal
syncytiotrophoblasts
using
single-nucleus
transcriptional
profiling
compare
stress
responses
preeclampsia.
For
characterization
syncytiotrophoblasts,
we
used
RNA
sequencing
platform,
single-cell
combinatorial
indexing
(sci-RNA-seq3),
profile
villi
fetal
membranes
from
unvaccinated
patients
symptomatic
at
birth
(n
=
4),
gestational
age-matched
controls
a
case
critical
second
trimester
delivery
term
1).
Clustering
nuclei
differential
gene
expression
analysis
was
performed
Seurat.
Gene
ontology
conducted
Enrichr.
High-confidence
target
identify
key
transcription
factor
nodes
governing
response
SARS-CoV-2
infection.
Bioinformatic
approaches
were
further
dataset
published
preeclampsia
signatures.
Tissue
analysis,
including
immunofluorescence,
validate
data
histology
for
an
expanded
cohort
placentas:
6),
asymptomatic
3),
5),
severe
features
7).
The
analyzed
comprised
15
cell
clusters
47,889
nuclei.
We
identified
3
representing
fusing
mature
overlapping
distinct
COVID-19.
analyses
indicated
that
following
alterations
syncytiotrophoblasts:
(1)
endoplasmic
reticulum
activation
signaling
pathways,
unfolded
protein
integrated
response;
(2)
regulation
by
CCAAT/enhancer-binding
beta
(CEBPB),
master
lineage;
(3)
upregulation
preeclampsia-associated
genes.
Using
complementary
methods,
confirmed
increased
levels
proteins
(eg,
BiP,
G3BP1)
(spliced
XBP1
mRNA),
CEBPB
(phosphorylation)
Increased
cytotrophoblast
proliferation
(Ki-67)
also
detected
COVID-19,
consistent
trophoblast
injury.
Markers
demonstrated
similarities
phenotype
Maternal
lineage
factor,
CEBPB.
Similarities
between
provide
insights
into
their
clinical
association.