medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 10, 2024
Abstract
Previous
studies
have
uncovered
genetic
loci
associated
with
celiac
disease
(CeD)
within
both
the
human
leukocyte
antigen
(HLA)
and
non-HLA
regions.
However,
half
of
heritability
remains
unexplained.
This
study
aimed
to
identify
novel
CeD
in
a
general
adult
population
screened
for
disease,
mitigating
likely
selection
bias
observed
previous
case-control
studies.
The
utilized
data
from
fourth
Trøndelag
Health
Study
(HUNT4)
Norway,
where
52,358
adults
were
using
serology,
identifying
465
previously
undiagnosed
biopsy-confirmed
cases.
Additionally,
377
diagnosed
cases
identified
through
hospital
journal
searches
registry
data.
Genotyping
373,185
single
nucleotide
polymorphisms
was
performed
on
all
participant
four
Illumina
HumanCoreExome
arrays.
Imputation,
Haplotype
Reference
Consortium
panel,
resulted
approximately
24.9
million
variants,
post
quality
control.
A
genome-wide
association
SAIGE,
functional
mapping
pathway
enrichment
analysis
conducted
FUMA.
All
except
one
42
known
autosomal
present
data,
which
seven
reached
suggestive
significance
threshold
(P
≤
5
×
10
−6
).
Thirteen
independent
associations
5×
−8
),
5p15.33
locus
showing
highest
potential
true
CeD,
warranting
further
validate
findings.
Notably,
IRX1
gene,
located
close
has
also
been
rheumatoid
arthritis,
suggesting
new
shared
autoimmune
locus.
The Lancet Regional Health - Europe,
Journal Year:
2025,
Volume and Issue:
50, P. 101201 - 101201
Published: Jan. 9, 2025
SummaryBackgroundCeliac
disease
(CeD)
may
be
associated
with
elevated
liver
enzymes.
However,
little
is
known
about
the
risk
of
chronic
(CLD)
various
etiologies
or
major
adverse
outcomes
(MALO)
in
CeD.
We
aimed
to
investigate
long-term
CLD
patients
CeD.MethodsSwedish
nationwide
cohort
study.
identified
48,027
biopsy-confirmed
CeD
between
1969
and
2017.
Each
patient
was
exactly
matched
≤5
general
population
reference
individuals
(n
=
231,909)
followed
through
2021.
Flexible
parametric
survival
models
estimated
adjusted
hazard
ratios
(aHRs)
any
specific
(i.e.,
viral
hepatitis,
metabolic
dysfunction-associated
steatotic
[MASLD],
alcohol-related
disease,
autoimmune
disease)
MALO
(compensated/decompensated
cirrhosis,
hepatocellular
carcinoma,
transplantation,
liver-related
death).FindingsDuring
a
median
follow-up
16.0
years,
649
1571
developed
(incidence
rate:
79.4
vs.
39.5/100,000
person-years).
had
higher
developing
than
(aHR
2.01,
95%CI:1.82−2.22).
This
remained
≥25
years
after
diagnosis,
giving
one
extra
case
per
110
until
then.
Positive
associations
were
present
for
4.86),
MASLD
2.54),
1.51).
Individuals
at
significantly
incident
1.54).
Sibling
comparisons
sensitivity
analyses
confirmed
main
findings.InterpretationCeD
persistently
increased
CLD,
although
absolute
low.
Physicians
should
vigilant
early
signs
dysfunction
CeD.FundingEuropean
Crohn's
Colitis
Organisation,
Swedish
Society
Medical
Research
(project#:
PG-23-0315-H-02),
FORTE
2016-00424),
Takeda,
Swiss
National
Science
Foundation
P500PM_210866).
Journal of Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
14(3), P. 725 - 725
Published: Jan. 23, 2025
Celiac
disease
(CeD),
also
known
as
gluten
enteropathy,
is
an
immune-mediated
inflammatory
enteropathy
triggered
by
intolerance
to
gluten.
It
presents
with
a
spectrum
of
symptoms,
including
both
gastrointestinal
and
extraintestinal
manifestations,
well
neurological
symptoms.
A
review
the
literature
indicates
that
10–22%
patients
CeD
present
The
objective
this
study
assess
influence
gluten-free
diet
(GFD)
on
brain
bioelectrical
activity
symptoms
in
children
CeD.
Methods:
was
conducted
using
multidisciplinary
approach,
encompassing
comprehensive
array
clinical
data
gathered
alongside
laboratory
test
results,
questionnaires,
electroencephalogram
(EEG)
assessments.
population
included
85
children:
18
newly
diagnosed
cases
(NDC),
subsequently
reassessed
after
6
months
GFD
celiac
(CDD);
27
for
over
12
(CDD2);
40
healthy
individuals
comparison
group
(CG).
Results:
observed
half
NDC
exhibited
particularly
headaches.
Following
six-month
period
GFD,
there
notable
reduction
symptom
severity.
In
CG,
patient
higher
prevalence
abnormalities
EEG
recordings
(p
=
0.032),
focal
sharp
waves
or
slow
waves.
Conclusions:
results
demonstrate
has
positive
impact
condition
improvements
correspond
normalization,
which
supports
hypothesis
dietary
intervention
plays
role
mitigating
CeD-associated
dysfunction.
Cells,
Journal Year:
2025,
Volume and Issue:
14(4), P. 279 - 279
Published: Feb. 14, 2025
Gliadin
is
one
of
the
most
important
fractions
gluten,
a
glycoprotein
closely
linked
to
development
negative
effects
on
physiological
functions
and
gastrointestinal
diseases,
such
as
celiac
disease
(CD).
Research
suggests
that
inadequate
stress
responses
anxiety
states
may
trigger
or
at
least
contribute
these
pathological
conditions.
Peritoneal
leukocytes
from
Prematurely
Aging
Mice
(PAM),
which
are
chronologically
adult
mice
with
compromised
anxiety,
exhibit
functional
changes
when
exposed
in
vitro
gliadin
peptides,
resembling
some
immune
alterations
found
also
CD
patients.
This
observation
prompted
us
investigate
gliadin-rich
diet
function
redox
state
PAM.
In
this
study,
female
PAM
were
fed
either
gluten-enriched
(PAMD,
120
g/kg)
standard
(PAMC)
for
four
weeks.
Immune
parameters
peritoneal,
splenic,
thymic
(phagocytosis,
chemotaxis,
Natural
Killer
activity,
lymphoproliferation)
markers
(glutathione
reductase,
glutathione
peroxidase,
reduced/oxidized
glutathione,
xanthine
oxidase
lipid
peroxidation)
evaluated.
The
results
showed
PAMD
exhibited
more
impaired
function,
lower
antioxidant
enzyme
activities,
reduced
concentrations,
well
higher
oxidized
increased
activity
compared
PAMC.
These
findings
suggest
worsens
impairments
PAM,
previously
described
CD,
indicating
potential
animal
studying
gluten-induced
dysregulation.
Gut,
Journal Year:
2025,
Volume and Issue:
unknown, P. gutjnl - 333589
Published: Feb. 17, 2025
Background
Oat
ingestion
in
coeliac
disease
(CD)
is
generally
regarded
as
safe
but
can
trigger
enteropathy
and
T
cells
specific
for
oat
avenin
the
gut
blood
of
some
individuals.
Objective
To
correlate
immune
clinical
outcomes
to
oats,
purified
feeding
studies
were
performed
examine
symptoms,
T-cell
immunity
intestinal
histology
CD.
Design
33
treated
HLA-DQ2.5+
adult
CD
patients
underwent
single-bolus
or
6-week
3-month
whole
oats
ingestion.
cell
activation
after
was
measured
using
serum
interleukin
2
(IL-2),
a
sensitive
biomarker
gluten-induced
symptoms
Symptom
measures,
histology,
on
duodenum
undertaken.
Results
Among
29
participants,
induced
dose-dependent
11
(38%)
acute
17
(59%).
Higher
IL-2
levels
correlated
with
more
severe
symptoms.
A
single
highly
symptomatic
patient
vomited
response
(1/29;
3%)
exhibited
striking
pro-inflammatory
cytokine
profile
similar
wheat-induced
responses.
Avenin
increased
frequency
CD38-expressing
tetramer+integrin
β7+
effector
memory
CD4+
blood,
however
release
tetramer
fell
following
intake
no
observed.
Conclusion
Gluten-contamination-free
symptom
responses
usually
at
level
insufficient
cause
sustained
enteropathy.
In
1
(3%)
triggered
wheat-like
response,
highlighting
that
minority
may
need
exclude
oats.
Informed
choice
regarding
important.
Journal of the Canadian Association of Gastroenterology,
Journal Year:
2025,
Volume and Issue:
8(Supplement_2), P. S51 - S55
Published: Feb. 21, 2025
Abstract
Celiac
disease
(CeD)
is
an
autoimmune
condition
driven
by
gluten
in
genetically
predisposed
individuals.
CeD
characterized
small
intestinal
villous
atrophy
but
presents
with
a
spectrum
of
gastrointestinal
and
systemic
manifestations.
Its
only
treatment
strict,
life-long
adherence
to
gluten-free
diet,
which
difficult
manage
does
not
always
lead
symptomatic
or
mucosal
recovery.
About
40%
the
population
express
CeD-associated
risk
genes,
1%-2%
worldwide
has
CeD.
This,
along
rising
prevalence
suggests
other
cofactors
pathogenesis.
The
gut
microbiome
been
implicated
based
on
epidemiology
studies
clinical
associations.
Mechanistic
using
relevant
vitro
vivo
preclinical
models
have
begun
elucidate
mechanisms
through
microbes
can
influence
Ultimately,
better
understanding
these
their
will
provide
rationale
intervention
strategies
novel
therapeutic
targets
prevent
treat
Science Translational Medicine,
Journal Year:
2025,
Volume and Issue:
17(790)
Published: March 19, 2025
Celiac
disease,
a
gluten-sensitive
enteropathy,
demonstrates
strong
human
leukocyte
antigen
(HLA)
association,
with
more
than
90%
of
patients
carrying
the
HLA-DQ2.5
allotype.
No
therapy
is
available
for
condition
except
lifelong
gluten-free
diet.
To
address
this
gap,
we
explored
therapeutic
potential
regulatory
T
cells
(Tregs).
By
orthotopic
replacement
cell
receptors
(TCRs)
through
homology-directed
repair,
generated
gluten-reactive
HLA-DQ2.5-restricted
CD4+
engineered
(e)
effector
(Teffs)
and
eTregs
performed
in
vivo
experiments
transgenic
mice.
Of
five
validated
TCRs,
TCRs
specific
two
immunodominant
deamidated
gluten
epitopes
(DQ2.5-glia-α1a
DQ2.5-glia-α2)
were
selected
further
evaluation.
eTeffs
exposed
to
oral
gavage
colocalized
dendritic
B
Peyer's
patches
gut-draining
lymph
nodes
specifically
migrated
intestine.
The
suppressive
function
correlated
high
TCR
functional
activity.
one
epitope
suppressed
proliferation
gut
migration
same
other
epitope,
demonstrating
bystander
suppression.
suppression
requires
an
antigen-specific
activation
given
that
polyclonal
Tregs
failed
suppress
eTeffs.
These
findings
highlight
as
celiac
disease.
European Journal of Inflammation,
Journal Year:
2025,
Volume and Issue:
23
Published: March 1, 2025
Primary
biliary
cholangitis
(PBC)
is
a
chronic
autoimmune
liver
disease
characterized
by
damage
to
small
intrahepatic
bile
ducts.
The
etiology
and
pathogenesis
of
PBC
remain
unknown.
It
often
considered
be
related
an
immunological
disorder
induced
genetics
environmental
factors.
Antimitochondrial
antibodies
(AMAs)
along
with
specific
antinuclear
such
as
gp210
Sp100
are
markers
the
disease.
Middle-aged
elderly
women
main
patients.
clinical
manifestations
non-specific,
which
presents
fatigue
skin
itching
usually.
However,
patients
gradually
develop
cholestasis
fibrosis,
eventually
dying
progressed
cirrhosis
failure.
Currently,
ursodeoxycholic
acid
(UDCA)
treatment
choice,
recommended
for
all
may
coexist
other
disorders
that
arise
from
multiple
systems,
inflammatory
bowel
(IBD),
Sjögren’s
syndrome
(SS)
type
1
diabetes
mellitus
(T1DM).
causal
relationship
between
extrahepatic
diseases
(EHAIDs)
unclear.
This
article
summarizes
new
developments
in
study
primary
aims
provide
reference
scientific
workers
field
research
on
this