Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 10, 2025
This
study
aimed
to
elucidate
the
transcriptomic
signatures
and
dysregulated
pathways
associated
with
autoimmune
response
in
Cd38
-/-
mice
compared
wild-type
(WT)
within
bm12
chronic
graft-versus-host
disease
(cGVHD)
lupus
model.
We
conducted
bulk
RNA
sequencing
on
peritoneal
exudate
cells
(PECs)
spleen
(SPC)
at
two
four
weeks
following
adoptive
cell
transfer.
also
analyzed
from
healthy,
untreated
mice.
These
analyses
revealed
a
sustained
upregulation
of
transcriptional
profile
purinergic
receptors
ectonucleotidases
cGVHD
WT
PECs,
which
displayed
coordinated
expression
several
type
I
interferon-stimulated
genes
(ISGs)
key
molecules
involved
cyclic
GMP-AMP
synthase-stimulator
interferon
(cGAS-STING)
signaling
pathway,
hallmarks
pathology.
A
second
receptor
profile,
included
P2rx7
P2rx4
,
showed
gene
components
NLRP3
inflammasome
its
potential
activators.
processes
were
transcriptionally
less
active
PECs
than
PECs.
have
shown
evidence
distinct
enrichment
that
define
such
as
Ca
2+
ion
homeostasis,
division,
phagosome,
autophagy,
senescence,
cytokine/cytokine
interactions,
Th17
Th1/Th2
differentiation
versus
samples,
reflected
milder
inflammatory
elicited
relative
counterparts
allogeneic
challenge.
Last,
we
an
intense
metabolic
reprogramming
toward
oxidative
phosphorylation
SPC
mice,
may
reflect
increased
cellular
demand
for
oxygen
consumption,
contrast
short-lived
effect
level.
Overall,
these
findings
support
pro-inflammatory
immunomodulatory
role
CD38
during
development
cGVHD-lupus
disease.
Journal of Clinical Investigation,
Год журнала:
2024,
Номер
134(17)
Опубликована: Июль 2, 2024
Cytomegalovirus
(CMV)
is
one
of
the
most
common
and
relevant
opportunistic
pathogens
in
people
who
are
immunocompromised,
such
as
kidney
transplant
recipients
(KTRs).
The
exact
mechanisms
underlying
disability
cytotoxic
T
cells
to
provide
sufficient
protection
against
CMV
immunosuppressed
have
not
been
identified
yet.
Here,
we
performed
in-depth
metabolic
profiling
CMV-specific
CD8+
patients
immunocompromised
show
development
dysregulation
at
transcriptional,
protein,
functional
level
KTRs
with
noncontrolled
infection.
These
dysregulations
comprise
impaired
glycolysis
increased
mitochondrial
stress,
which
associated
an
intensified
expression
nicotinamide
adenine
dinucleotide
nucleotidase
(NADase)
CD38.
Inhibiting
NADase
activity
CD38
reinvigorated
metabolism
improved
cytokine
production
cells.
findings
were
corroborated
a
mouse
model
infection
under
conditions
immunosuppression.
Thus,
dysregulated
states
could
be
targeted
by
inhibiting
reverse
hyporesponsiveness
individuals
fail
control
chronic
viral
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(20), С. 10905 - 10905
Опубликована: Окт. 10, 2024
Systemic
lupus
erythematosus
(SLE)
is
a
complex
autoimmune
disease,
characterized
by
considerable
changes
in
peripheral
lymphocyte
structure
and
function,
that
plays
critical
role
commencing
reviving
the
inflammatory
immune
signaling
pathways.
In
healthy
individuals,
B
lymphocytes
have
major
guiding
directing
defense
mechanisms
against
pathogens.
Certain
phenotype,
including
alterations
surface
endosomal
receptors,
occur
presence
of
SLE
lead
to
dysregulation
subpopulations.
Functional
are
loss
self-tolerance,
intra-
extrafollicular
activation,
increased
cytokine
autoantibody
production.
T
seem
supporting,
rather
than
leading,
disease
pathogenesis.
Substantial
aberrations
subsets
evident,
include
reduction
cytotoxic,
regulatory,
advanced
differentiated
subtypes,
together
with
an
increase
activated
autoreactive
forms
abnormalities
follicular
cells.
Up-regulated
subpopulations,
such
as
central
effector
memory
cells,
produce
pre-inflammatory
cytokines,
activate
lymphocytes,
stimulate
cell
This
review
explores
pivotal
roles
pathogenesis
Lupus
Nephritis,
emphasizing
multifaceted
interactions
their
phenotypic
functional
dysregulations.
Lupus Science & Medicine,
Год журнала:
2025,
Номер
12(1), С. e001368 - e001368
Опубликована: Фев. 1, 2025
Background
SLE
is
associated
with
significant
morbidity,
especially
in
the
case
of
renal
involvement.
Mitochondrial
dysfunction
plays
a
role
and
may
be
assessed
by
measuring
mitochondrial
DNA
(mtDNA)
cytokines
reflecting
stress
(mitokines).
Circulating
mtDNA
promising
biomarker
appears
to
reduced
severe
SLE.
However,
circulating
challenging
reported
methods
are
heterogenous.
Our
study
aimed
at
evaluating
whole
blood
nuclear
(nucDNA)
ratio
using
droplet-digital
PCR
mitokines,
growth
differentiation
factor
15
(GDF-15)
fibroblast
21
without
Methods
Cross-sectional
involving
195
patients
age-matched
healthy
volunteers
(HV)
as
control.
Biomarkers
were
compared
involvement
(defined
estimated
glomerular
filtration
rate
<60
mL/min
or
proteinuria
>0.5
g/day)
those
active
inactive
Results
Compared
HV,
displayed
lower
mtDNA/nucDNA
ratios,
Accordingly,
mitokines
increased
We
found
no
correlation
between
global
disease
activity.
Mitokine
levels,
on
other
hand,
correlated
activity,
particular
GDF-15
even
after
adjusting
for
Conclusion
findings
suggest
that
ratio,
surrogate
marker
dysfunction,
reflects
damage,
while
also
reflect
activity
Further
studies
needed
assess
clinical
value
these
markers
predictors
lupus
nephritis.
Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 10, 2025
This
study
aimed
to
elucidate
the
transcriptomic
signatures
and
dysregulated
pathways
associated
with
autoimmune
response
in
Cd38
-/-
mice
compared
wild-type
(WT)
within
bm12
chronic
graft-versus-host
disease
(cGVHD)
lupus
model.
We
conducted
bulk
RNA
sequencing
on
peritoneal
exudate
cells
(PECs)
spleen
(SPC)
at
two
four
weeks
following
adoptive
cell
transfer.
also
analyzed
from
healthy,
untreated
mice.
These
analyses
revealed
a
sustained
upregulation
of
transcriptional
profile
purinergic
receptors
ectonucleotidases
cGVHD
WT
PECs,
which
displayed
coordinated
expression
several
type
I
interferon-stimulated
genes
(ISGs)
key
molecules
involved
cyclic
GMP-AMP
synthase-stimulator
interferon
(cGAS-STING)
signaling
pathway,
hallmarks
pathology.
A
second
receptor
profile,
included
P2rx7
P2rx4
,
showed
gene
components
NLRP3
inflammasome
its
potential
activators.
processes
were
transcriptionally
less
active
PECs
than
PECs.
have
shown
evidence
distinct
enrichment
that
define
such
as
Ca
2+
ion
homeostasis,
division,
phagosome,
autophagy,
senescence,
cytokine/cytokine
interactions,
Th17
Th1/Th2
differentiation
versus
samples,
reflected
milder
inflammatory
elicited
relative
counterparts
allogeneic
challenge.
Last,
we
an
intense
metabolic
reprogramming
toward
oxidative
phosphorylation
SPC
mice,
may
reflect
increased
cellular
demand
for
oxygen
consumption,
contrast
short-lived
effect
level.
Overall,
these
findings
support
pro-inflammatory
immunomodulatory
role
CD38
during
development
cGVHD-lupus
disease.