Clinical & Translational Immunology,
Год журнала:
2024,
Номер
13(12)
Опубликована: Янв. 1, 2024
Type
2
epithelial
cytokines,
including
thymic
stromal
lymphopoietin
and
IL-33,
play
central
roles
in
modulation
of
type
immune
cells,
such
as
basophils.
Basophils
are
a
small
subset
granulocytes
within
the
leukocyte
population
that
predominantly
exist
blood.
They
have
non-redundant
allergic
inflammation
peripheral
tissues
lung,
skin
gut,
where
they
increase
accumulate
at
inflammatory
lesions
exclusively
produce
large
amounts
IL-4,
cytokine.
These
reactions
known
to
be,
some
extent,
phenocopies
infectious
diseases
ticks
helminths.
Recently,
biologics
related
both
cytokines
basophils
been
approved
by
US
Food
Drug
Administration
for
treatment
diseases.
We
summarised
basic
science
translational
medicine,
recent
findings.
Immunological Reviews,
Год журнала:
2025,
Номер
331(1)
Опубликована: Март 31, 2025
Type
2-mediated
immune
responses
protect
the
body
against
environmental
threats
at
barrier
surfaces,
such
as
large
parasites
and
toxins,
facilitate
repair
of
inflammatory
tissue
damage.
However,
maladaptive
to
typically
nonpathogenic
substances,
commonly
known
allergens,
can
lead
development
allergic
diseases.
2
immunity
involves
a
series
prototype
TH2
cytokines
(IL-4,
IL-5,
IL-13)
alarmins
(IL-33,
TSLP)
that
promote
generation
adaptive
CD4+
helper
cells
humoral
products
allergen-specific
IgE.
Mast
basophils
are
integral
players
in
this
network,
serving
primary
effectors
IgE-mediated
responses.
These
bind
IgE
via
high-affinity
receptors
(FcεRI)
expressed
on
their
surface
and,
upon
activation
by
release
variety
mediators
regulate
responses,
attract
modulate
other
cells,
contribute
repair.
Here,
we
review
biology
effector
mechanisms
these
focusing
primarily
role
mediating
both
physiological
pathological
contexts.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(14), С. 7910 - 7910
Опубликована: Июль 19, 2024
Difamilast,
a
phosphodiesterase
4
(PDE4)
inhibitor,
has
been
shown
to
be
effective
in
the
treatment
of
atopic
dermatitis
(AD),
although
mechanism
involved
remains
unclear.
Since
IL-33
plays
an
important
role
pathogenesis
AD,
we
investigated
effect
difamilast
on
activity.
vitro
model
cultured
normal
human
epidermal
keratinocytes
(NHEKs)
utilized
evaluate
pharmacological
potential
adjunctive
treated
NHEKs
with
and
analyzed
expression
suppression
tumorigenicity
2
protein
(ST2),
receptor
transmembrane
(ST2L)
soluble
(sST2)
isoforms.
Difamilast
increased
mRNA
levels
sST2,
decoy
suppressing
signal
transduction,
without
affecting
ST2L
expression.
Furthermore,
supernatants
from
difamilast-treated
inhibited
IL-33-induced
upregulation
TNF-α,
IL-5,
IL-13
KU812
cells,
basophil
cell
line
sensitive
IL-33.
We
also
found
that
activated
aryl
hydrocarbon
(AHR)-nuclear
factor
erythroid
2-related
(NRF2)
axis.
Additionally,
knockdown
AHR
or
NRF2
abolished
difamilast-induced
sST2
production.
These
results
indicate
produces
via
AHR-NRF2
axis,
contributing
improving
AD
symptoms
by
inhibiting
Abstract
The
skin
serves
as
the
first
protective
barrier
for
nonspecific
immunity
and
encompasses
a
vast
network
of
skin‐associated
immune
cells.
Atopic
dermatitis
(AD)
is
prevalent
inflammatory
disease
that
affects
individuals
all
ages
races,
with
complex
pathogenesis
intricately
linked
to
genetic,
environmental
factors,
dysfunction
well
dysfunction.
Individuals
diagnosed
AD
frequently
exhibit
genetic
predispositions,
characterized
by
mutations
impact
structural
integrity
barrier.
This
leads
release
alarmins,
activating
type
2
pathway
recruiting
various
cells
skin,
where
they
coordinate
cutaneous
responses.
In
this
review,
we
summarize
experimental
models
provide
an
overview
its
therapeutic
interventions.
We
focus
on
elucidating
intricate
interplay
between
system
regulatory
mechanisms,
commonly
used
treatments
AD,
aiming
systematically
understand
cellular
molecular
crosstalk
in
AD‐affected
skin.
Our
overarching
objective
novel
insights
inform
potential
clinical
interventions
reduce
incidence
AD.
Current Medical Research and Opinion,
Год журнала:
2024,
Номер
40(5), С. 753 - 763
Опубликована: Апрель 16, 2024
Atopic
dermatitis
(AD)
has
become
a
common
childhood
disease
that
affects
large
number
of
children
worldwide
and
chronic
skin
cause
huge
economical
psychological
damage
to
the
whole
family.
Despite
use
steroids,
immunosuppressants
various
topical
preparation,
prognosis
is
still
poor.
Hence,
this
review
aimed
explore
potential
using
essential
oils
(EO)
as
an
active
ingredient
in
managing
AD.
The
was
completed
by
Pubmed,
Scopus
Medline
search
for
relevant
articles
study
pathophysiology
AD,
properties
EO,
EO
AD
suitable
advanced
formulation
incorporate
EO.
From
conducted,
it
concluded
can
be
used
complimentary
therapeutic
agents
treatment.
Scientists
industries
should
venture
into
commercialising
more
products
with
help
manage
effectively.
Dermatology and Therapy,
Год журнала:
2024,
Номер
14(9), С. 2443 - 2455
Опубликована: Июль 29, 2024
Difamilast
is
the
first
selective
phosphodiesterase
4
inhibitor
approved
for
atopic
dermatitis
(AD)
in
Japan.
A
phase
3,
52-week,
open-label
study
ongoing
to
establish
efficacy
and
safety
of
difamilast
ointments
infants
with
AD
aged
3
<
24
months
because
a
clinical
has
not
been
conducted
this
population.
This
consisted
4-week
primary
evaluation
period
which
0.3%
ointment
was
applied
twice
daily
Japanese
(n
=
41)
an
48-week
long-term
extension
or
1%
based
on
existing
symptoms.
The
data
were
obtained
as
interim
report
period.
response
rate
Investigator's
Global
Assessment
score
45.0%
at
week
1,
maintained
56.1%
63.4%
report.
Infants
achieved
Eczema
Area
Severity
Index
75
(improvement
≥
75%)
47.5%
further
improved
82.9%
78.1%
Adverse
events
(AEs)
reported
22
(53.7%)
period:
those
most
frequent
AE
nasopharyngitis
(19.5%)
followed
by
contact
(7.3%).
As
report,
36
(87.8%)
experienced
AEs:
those,
(70.7%)
gastroenteritis
(22.0%)
frequently
observed.
total
AEs
mostly
mild
moderate
severity.
No
investigational
medicinal
product-related
no
leading
discontinuation
reported.
effective
well
tolerated
final
results
will
be
near
future.
Clinical
Trial
Registration:
Trials.
gov
identifier:
NCT05372653.
