No allergy, but mast cells are involved: MRGPRX2 in chronic inflammatory skin diseases
Journal of the European Academy of Dermatology and Venereology,
Год журнала:
2025,
Номер
39(3), С. 451 - 452
Опубликована: Фев. 25, 2025
Язык: Английский
Histamine H3 and H4 Receptor Antagonists Differentially Inhibit Mast Cell Activation via FcεRI and MRGPRX2 Pathways
Clinical & Experimental Allergy,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 2, 2025
Язык: Английский
Psychological Stress and Urticaria: Pathophysiologic and Therapeutic Updates
Current Treatment Options in Allergy,
Год журнала:
2024,
Номер
unknown
Опубликована: Сен. 20, 2024
Язык: Английский
Role of Platelet-Activating Factor in the Pathogenesis of Chronic Spontaneous Urticaria
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(22), С. 12143 - 12143
Опубликована: Ноя. 12, 2024
Chronic
spontaneous
urticaria
(CSU)
is
a
debilitating
condition
characterized
by
mast
cell
activation.
Platelet-activating
factor
(PAF)
produced
various
immune
cells,
including
basophils,
lymphocytes,
and
eosinophils,
which
play
crucial
roles
in
CSU
pathogenesis.
It
induces
degranulation,
increases
vascular
permeability,
promotes
the
chemotaxis
of
inflammatory
cells.
These
effects
result
release
mediators,
development
edema,
persistence
inflammation,
are
key
features
CSU.
Notably,
elevated
PAF
levels
have
been
linked
to
heightened
disease
activity
resistance
antihistamine
treatment
patients.
Despite
these
findings,
precise
role
pathogenesis
remains
unclear.
Rupatadine,
an
antihistamine,
heat
shock
protein
10,
natural
anti-inflammatory
peptide
that
selectively
inhibits
PAF-induced
demonstrated
anti-PAF
activity.
Furthermore,
with
molecular
structure
receptor
now
identified,
several
experimental
antagonists
synthesized.
However,
there
significant
need
for
therapeutic
options
targeting
management.
Язык: Английский
IL-27 as a novel biomarker for pruritus in nodular prurigo and bullous pemphigoid
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Дек. 13, 2024
Introduction
Bullous
pemphigoid
(BP)
and
prurigo
nodularis
(PN)
are
chronic
pruritic
skin
diseases
that
severely
impact
patients’
quality
of
life.
Despite
the
widespread
attention
these
two
have
garnered
within
dermatological
field,
specific
pathogenesis,
particularly
molecular
mechanisms
underlying
pruritus,
remains
largely
unclear.
Limited
clinical
sequencing
studies
focusing
on
BP
PN
hindered
identification
pathological
exploration
effective
treatment
strategies.
Methods
To
address
this
gap,
we
collected
a
total
23
peripheral
blood
mononuclear
cell
samples
from
patients,
as
well
healthy
controls,
performed
RNA
analysis.
By
integrating
bioinformatics
machine
learning
techniques,
aimed
to
uncover
shared
immune
regulatory
networks
pruritus-related
between
PN.
Results
Our
study
identified
161
differentially
expressed
genes
PN,
which
were
primarily
enriched
in
activation
neural
pathways,
providing
crucial
insights
into
both
diseases.
Furthermore,
using
algorithms
support
vector
machines
random
forest,
pinpoint
7
databases.
Among
these,
IL-27
emerged
potential
pivotal
gene,
its
mRNA
expression
levels
strongly
correlated
with
parameters
including
pruritus
scores,
immunoglobulin
E
levels,
eosinophil
counts.
Validation
experiments
conducted
an
additional
22
participants
confirmed
upregulation
lesions.
Discussion
This
is
first
unveil
inflammatory
pathways
common
highlighting
critical
role
pathogenesis
conditions.
findings
not
only
enhance
understanding
intricate
relationship
but
also
provide
foundation
for
development
novel
therapeutic
strategies
targeting
Язык: Английский