Current Opinion in Rheumatology,
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 8, 2024
Aberrant
autoreactive
innate
and
adaptive
immune
responses
cause
systemic
autoimmune
diseases.
Autoimmunity
has
been
linked
to
abnormal
metabolic
states,
immunometabolism
emerged
as
a
critical
field
in
understanding
the
pathogenesis
of
rheumatic
We
aimed
explore
latest
research
on
reprogramming
various
cell
types,
including
T
cells,
B
neutrophils,
dendritic
monocytes,
macrophages,
context
Clinical and Translational Medicine,
Год журнала:
2024,
Номер
14(3)
Опубликована: Март 1, 2024
The
interplay
between
the
immune
system
and
metabolic
state
of
a
cell
is
intricate.
In
all
phases
an
response,
corresponding
changes
shall
occur
to
support
its
modulation,
in
addition
signalling
through
cytokine
environment
receptor
stimulation.
While
autoimmune
disorders
may
develop
because
imbalance
that
modulates
switching
T-cell
phenotypes,
effects
interaction
T
B
cells
have
on
one
another's
cellular
metabolism
are
yet
be
understood
disease
context.
Here,
we
propose
perspective
which
highlights
potential
targeting
modulate
T-
B-cell
subtypes
populations
as
well
T-B
B-T
interactions
successfully
treat
disorders.
Specifically,
envision
how
can
tip
balance
interactions,
definite
mechanisms
both
health
disease,
explain
phenotype
switches
cells.
Within
this
scenario,
highlight
link
inflammation,
immunometabolism,
epigenetics
ageing,
critical
understand
inflammatory
combination
treatments
cause
(T/B)
imbalances,
pathways
involved,
increase
effectiveness
treatment
disorders,
and/or
ameliorate
their
symptoms
improve
patients'
quality
life.
Biomolecules,
Год журнала:
2025,
Номер
15(3), С. 332 - 332
Опубликована: Фев. 25, 2025
Type
1
diabetes
(T1D)
is
an
autoimmune
disease
that
affects
estimated
30
million
people
worldwide
and
results
in
a
lifelong
dependency
of
exogenous
insulin
treatments.
While
T1D
characterized
by
T-cell
driven-destruction
the
insulin-secreting
β
cells,
B
lymphocytes
play
key
role
islet–immune
interface.
cells
are
essential
intermediary
between
islet
other
immune-cell
populations.
Through
antigen
presentation,
cytokine
secretion,
antibody
production,
activating
autoreactive
islet-specific
T
thus
potentiating
pancreatic
inflammation
early
stages
T1D.
Despite
this,
their
development
remains
understudied
feature
with
significant
therapeutic
potential.
Herein,
we
will
discuss
current
knowledge
islet–immune-cell
interface
within
through
lens
lymphocytes.
We
also
consider
gaps
may
be
limiting
further
opportunities.
Journal of Inflammation Research,
Год журнала:
2025,
Номер
Volume 18, С. 3105 - 3123
Опубликована: Март 1, 2025
Friend
Leukemia
Integration
1
Transcription
Factor
(FLI1)
has
attracted
attention
due
to
its
involvement
in
rheumatoid
arthritis
(RA).
Nevertheless,
the
precise
mechanism
through
which
FLI1
contributes
RA
remains
elusive.
We
investigated
potential
role
of
integrated
bioinformatics,
clinical
experiments,
and
cellular
experiments.
Based
on
GSE1919
GSE12021
datasets,
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
Gene
Ontology
(GO)
analyses
identified
as
a
differential
gene
RA.
Clinical
validation
was
performed
by
measuring
expression
serum
collected
from
patients.
Correlational
analysis
between
immune-inflammatory
markers
confirmed
association
with
inflammation.
WGCNA
analysis,
along
KnockTF,
JASPAR,
ENCODE
databases,
employed
predict
target
genes
FLI1.
Receiver
operating
characteristic
gene-set
enrichment
analysis-KEGG
were
conducted
elucidate
biological
functions
these
genes.
Finally,
experiments
validate
FLI1's
regulatory
effects
impact
synovial
cell
viability
apoptosis
upregulated
exhibited
positive
correlations
CRP,
ESR,
CCP,
RF,
IL-6,
IL-10,
IL-8,
TNF-α.
The
combined
detection
RF
demonstrated
highest
efficacy
evaluating
disease
activity.
most
strongly
associated
AGA,
DCK,
LRRC15,
MAN2A1,
TES,
all
suppression
led
decreased
TES.
Furthermore,
inhibition
reduced
cells
promoted
their
apoptosis.
FLI
is
can
promote
inflammation,
increase
viability,
or
inhibit
This
finding
suggests
that
may
serve
novel
therapeutic
targets
present
findings
integrate
bioinformatics
experimental
approaches
advance
our
current
understanding
open
new
avenues
for
targeted
therapies.
Communications Biology,
Год журнала:
2025,
Номер
8(1)
Опубликована: Март 10, 2025
Membranous
nephropathy
(MN)
is
a
primary
glomerular
disease
commonly
causing
adult
nephrotic
syndrome.
Characterized
by
thickened
capillary
walls
due
to
immune
complex
deposition,
MN
autoimmune
disorder.
Its
pathogenesis
involves
deposit
formation,
complement
activation,
and
heightened
risk
of
renal
failure.
Central
system
dysfunction,
particularly
the
dysregulation
B
T
cell
responses.
cells
contribute
injury
through
production
autoantibodies,
IgG
targeting
phospholipase
A2
receptor
(PLA2R)
on
podocytes,
while
modulate
responses
that
influence
progression.
Metabolic
reprogramming
alters
lymphocyte
survival,
differentiation,
proliferation,
function,
potentially
triggering
processes.
Although
link
between
metabolism
remains
underexplored,
this
review
highlights
recent
advances
in
understanding
its
role
MN.
These
insights
may
provide
novel
biomarkers
therapeutic
strategies
for
treatment.
Immune
membranous
drives
Dysregulated
B/T
metabolic
trigger
autoimmunity,
offering
potential
therapies
Abstract
Antibodies
are
essential
to
immune
homeostasis
due
their
roles
in
neutralizing
pathogenic
agents.
However,
failures
central
and
peripheral
checkpoints
that
eliminate
autoreactive
B
cells
can
undermine
self-tolerance
generate
autoantibodies
mistakenly
target
self-antigens,
leading
inflammation
autoimmune
diseases.
While
well-studied
some
communicable
diseases,
chronic
conditions,
such
as
obesity
aging,
less
understood.
Obesity
aging
share
similar
aspects
of
dysfunction,
diminished
humoral
responses
heightened
inflammation,
which
disrupt
tolerance
foster
autoantigen
production,
thus
giving
rise
autoantibodies.
In
return,
these
events
may
also
contribute
the
pathophysiology
associated
disorders
linked
development
immunosenescence,
an
age-related
decline
function
heightens
vulnerability
infections,
loss
self-tolerance.
Furthermore,
cumulative
exposure
antigens
cellular
debris
during
perpetuates
pro-inflammatory
pathways,
linking
immunosenescence
with
other
hallmarks,
proteostasis
mitochondrial
dysfunction.
This
review
examines
mechanisms
driving
autoantibody
generation
discusses
key
putative
antigenic
targets
across
conditions.
We
explore
therapeutic
potential
emerging
approaches,
CAR-T/CAAR-T
therapies,
vaccines,
BiTEs,
tackle
autoimmune-related
conditions
obesity.
Heliyon,
Год журнала:
2024,
Номер
10(17), С. e36220 - e36220
Опубликована: Авг. 15, 2024
Sjögren's
syndrome
(SS)
is
a
chronic
autoimmune
disease
that
affects
the
exocrine
glands
and
may
lead
to
range
of
systemic
symptoms
impact
various
organs.
Both
innate
adaptive
immune
pathways
might
trigger
disease.
Studying
signaling
underlying
SS
crucial
for
enhancing
diagnostic
therapeutic
effectiveness.
poses
an
ongoing
challenge
medical
professionals
owing
limited
options
available.
This
review
offers
comprehensive
understanding
intricate
nature
SS,
encompassing
classification
criteria,
risk
factors,
in
immunity
inflammation.
The
advancements
summarized
herein
have
potential
spark
new
avenues
research
into
SS.
