A Comprehensive Review of Fc Gamma Receptors and Their Role in Systemic Lupus Erythematosus
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(5), P. 1851 - 1851
Published: Feb. 21, 2025
Receptors
for
the
immunoglobulin
G
constant
fraction
(FcγRs)
are
widely
expressed
in
cells
of
immune
system.
Complement-independent
phagocytosis
prompted
FcγR
research
to
show
that
engagement
IgG
complexes
with
FcγRs
triggers
a
variety
cell
host
responses,
such
as
phagocytosis,
antibody-dependent
cytotoxicity,
and
NETosis,
among
others.
However,
variants
these
receptors
have
been
implicated
development
susceptibility
autoimmune
diseases
systemic
lupus
erythematosus.
Currently,
knowledge
is
required
field
antibody
therapeutics,
which
includes
engineering
recombinant
soluble
human
Fc
gamma
receptors,
enhancing
inhibitory
blocking
activating
function,
vaccines,
organ
transplantation.
Importantly,
recent
interest
enhancement
(ADE),
mechanism
by
pathogenesis
certain
viral
infections
enhanced.
ADEs
may
be
responsible
severity
SARS-CoV-2
infection.
Therefore,
become
current
topic.
this
review
briefly
describes
some
historical
about
type
I
family
humans,
including
structure,
affinity,
ligand
binding,
erythematosus
(SLE),
potential
therapeutic
approaches
related
SLE.
Language: Английский
Aging-induced dysbiosis worsens sepsis severity but is attenuated by probiotics in D-galactose-administered mice with cecal ligation and puncture model
Chalisa Pinitchun,
No information about this author
Wimonrat Panpetch,
No information about this author
Thansita Bhunyakarnjanarat
No information about this author
et al.
PLoS ONE,
Journal Year:
2024,
Volume and Issue:
19(10), P. e0311774 - e0311774
Published: Oct. 18, 2024
Introduction
Despite
the
well-established
effects
of
aging
on
brain
function
and
gut
dysbiosis
(an
imbalance
in
microbiota),
influence
sepsis-associated
encephalopathy
(SAE)
role
probiotics
this
context
remain
less
understood.
Methods
C57BL/6J
mice
(8-week-old)
were
subcutaneously
administered
with
8
weeks
D-galactose
(D-gal)
or
phosphate
buffer
solution
(PBS)
for
non-aging
models,
respectively,
without
oral
Lacticaseibacillus
rhamnosus
GG
(LGG).
Additionally,
impact
condition
media
from
LGG
(LCM)
was
tested
macrophages
(RAW
264.7
cells),
microglia
(BV-2
hippocampal
cells
(HT-22
cells).
Result
Fecal
microbiome
analysis
demonstrated
D-gal-induced
(reduced
Firmicutes
Desulfobacterota
increased
Bacteroidota
Verrucomicrobiota),
which
partially
neutralized
dysbiosis.
D-gal
also
worsens
cecal
ligation
puncture
(CLP)
sepsis
severity
when
compared
PBS-CLP
mice,
as
indicated
by
serum
creatinine
(Scr)
alanine
transaminase
(ALT),
but
not
mortality,
neurological
characteristics
(SHIRPA
score),
cytokines
(TNF-α
IL-6).
supported
fibrosis
liver,
kidney,
lung;
however,
CLP
did
worsen
fibrosis.
Interestingly,
attenuated
all
parameters
(mortality,
Scr,
ALT,
SHIRPA,
cytokines)
(PBS-CLP)
while
improving
these
parameters,
except
mortality
IL-6,
(D-gal
CLP).
For
vitro
test
using
lipopolysaccharide
(LPS)
stimulation,
LCM
inflammation
some
RAW264.7
BV-2
HT-22
cells,
implying
a
direct
anti-inflammatory
effect
macrophages,
brain.
Conclusion
induced
fecal
worsened
determined
Scr
could
alleviate
most
selected
sepsis,
including
SAE.
However,
SAE
delivery
beneficial
molecules
to
partly
due
attenuation
systemic
through
modulation
macrophages.
Language: Английский
Intratracheal Candida administration induced lung dysbiosis, activated neutrophils, and worsened lung hemorrhage in pristane-induced lupus mice
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: March 21, 2025
Because
the
innate
immunity
might
and
fungi
in
lungs
enhance
severity
of
lupus-induced
diffuse
alveolar
hemorrhage
(DAH),
intraperitoneal
pristane
injection
was
performed
C57BL6
mice
with
intratracheal
administration
by
Candida
albicans
or
phosphate
buffer
solution
(PBS).
Despite
similar
pristane-induced
lupus
(proteinuria,
serum
creatinine,
anti-dsDNA)
at
5
weeks
model,
worsened
several
characteristics,
including
mortality,
body
weight,
cytokines
(TNF-α
IL-6),
lung
score,
tissue
(TNF-α,
IL-6,
IL-10),
but
not
gut
permeability
(FITC-dextran
assay),
IL-10,
immune
cells
spleens
(flow
cytometry
analysis),
activities
peritoneal
macrophages
(polymerase-chain
reaction).
Although
reduced
proteobacterial
abundance
altered
alpha
beta
diversity
compared
PBS
control,
microbiota
different
between
pristane-
non-pristane-administered
mice.
prominent
Gram-negative
bacteria
role
neutrophils
DAH,
lipopolysaccharide
(LPS)
without
heat-killed
preparation
tested.
Indeed,
LPS
induced
more
severe
pro-inflammatory
than
stimulation
alone
as
indicated
expression
genes
IL-1β,
Dectin-1,
NF-κB).
In
conclusion,
partly
through
enhanced
neutrophil
responses
against
fungi.
More
studies
on
colonization
sputum
from
patients
DAH
are
interesting.
Language: Английский
Alcohol-induced gut permeability defect through dysbiosis and enterocytic mitochondrial interference causing pro-inflammatory macrophages in a dose dependent manner
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: April 27, 2025
Although
toxicity
of
alcohol
toward
the
intestines
and
immunity
is
mentioned,
there
might
be
different
effect
in
a
low
high
dose
rodent
model
development
using
simple
SHIRPA
binary
score
night
useful.
Hence,
(6.30
1.26
g/kg/day)
were
administered
for
16
weeks
before
determination
several
parameters.
As
such,
peak
blood
concentration
(BAC)
approximately
at
0.05
0.15%,
respectively,
1
h
post-administration,
which
correlated
with
1.8
±
0.8
7.2
0.6,
respectively.
After
wk
administration,
significant
liver
injury
high-dose
was
indicated
by
enzymes,
weight,
histology
score,
apoptosis,
hepatic
accumulation
triglyceride
(TG)
oxidative
stress
(malondialdehyde;
MDA)
reduced
anti-oxidant
(glutathione).
Meanwhile,
low-dose
demonstrated
only
elevated
apoptosis
increased
TG
MDA
tissue.
Leaky
gut
from
both
also
FITC-dextran,
endotoxemia,
serum
beta
glucan,
occludin.
However,
bacterial
abundance
(microbiome
analysis)
feces
small
bowel
alcohol,
but
not
dose,
control
(increased
Alitipes
spp.
Lachnospiraceae).
In
conclusion,
low-
induced
leaky
gut,
while
caused
dysbiosis
damaged
mitochondria
enhanced
glycolysis
enterocytes
macrophages.
more
sensitive
than
to
determine
alcohol-induced
intestinal
injury.
Language: Английский
Accelerating and protective effects toward cancer growth in cGAS and FcgRIIb deficient mice, respectively, an impact of macrophage polarization
Arthid Thim-uam,
No information about this author
Papasara Chantawichitwong,
No information about this author
Pornpimol Phuengmaung
No information about this author
et al.
Inflammation Research,
Journal Year:
2025,
Volume and Issue:
74(1)
Published: April 24, 2025
Language: Английский
Alterations of the gut microbiota in the lupus nephritis: a systematic review
Anjing Wang,
No information about this author
Jin Zhao,
No information about this author
Yunlong Qin
No information about this author
et al.
Renal Failure,
Journal Year:
2023,
Volume and Issue:
45(2)
Published: Nov. 23, 2023
Background
Emerging
evidence
suggests
that
gut
microbiota
dysbiosis
may
play
a
critical
role
in
the
development
of
lupus
nephritis
(LN).
However,
specific
characteristics
individuals
with
LN
have
not
been
fully
clarified.
Language: Английский
Comparative time-series analyses of gut microbiome profiles in genetically and chemically induced lupus-prone mice and the impacts of fecal transplantation
Piraya Chatthanathon,
No information about this author
Asada Leelahavanichkul,
No information about this author
Thanya Cheibchalard
No information about this author
et al.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Nov. 2, 2024
Although
the
association
between
gut
dysbiosis
(imbalance
of
microbiota)
in
systemic
lupus
erythematosus
(SLE)
is
well-known,
simultaneous
exploration
fecal
and
different
intestinal
sections
before
after
onset
(at
2,
4,
6,
8,
10
months
old)
resulting
from
loss
inhibitory
Fc
gamma
receptor
IIb
(FcGIIb)
pristane
induction
have
never
been
conducted.
Anti-dsDNA
(an
important
autoantibody)
proteinuria
developed
as
early
6
old
both
models,
with
higher
levels
FcGRIIb
deficient
(FcGRIIb-/-)
mice.
Compared
to
healthy
control
at
2
4
months,
mice
(both
FcGRRIIb-/-
pristane)
demonstrated
an
alteration
indicated
by
Shannon
alpha
diversity
index,
highlighting
influences
lupus-
age-induced
dysbiosis,
respectively.
Non-metric
multidimensional
scaling
(NMDS)
revealed
that
microbiota
FcGRIIb-/-
were
distinct
age-matched
all
timepoints
month,
p
<
0.05),
while
showed
divergence
only
some
timepoints.
Analyses
similarity
among
cecum,
colon,
feces,
contrasting
those
small
intestines
(duodenum,
jejunum,
ileum).
Subtle
differences
found
feces
assessed
several
analyses,
for
examples,
similar
or
dissimilar
distances
(NMDS),
neighbor-joining
clustering,
potential
metabolisms
(KEGG
pathway
analysis).
Due
(feces
sections)
control,
rebalancing
using
rectal
administration
(fecal
transplantation;
FMT)
7-month-old
FcGIIb-/-
(the
established
lupus;
positive
anti-dsDNA
proteinuria)
was
performed.
In
comparison
without
FMT,
FMT
(more
effect
on
female
than
male
mice)
lower
microbiome
(16s
DNA
gene
copy
number)
patterns
control.
conclusion,
(FcGRIIb-/-
diverged
4-6
old,
correlating
characteristics
(anti-dsDNA
proteinuria).
The
suggested
a
possible
various
molecular
causes.
Furthermore,
appeared
mitigate
reduce
anti-dsDNA,
supporting
benefit
lupus,
more
studies
are
warranted.
Language: Английский