Scientific Reports,
Год журнала:
2024,
Номер
14(1)
Опубликована: Окт. 18, 2024
While
Coronavirus
disease
2019
(COVID-19)
vaccines
have
proven
to
be
both
effective
and
generally
safe,
rare
but
severe
adverse
events
following
immunization
(AEFIs)
are
described.
Autoantibodies
platelet
factor-4
associated
with
catastrophic
thrombotic
AEFIs,
comprehensive
investigations
of
other
autoantibodies
lacking.
We
aimed
detect
describe
targeting
coagulation-related
proteins
in
a
population-wide
cohort
(SWEDEGENE)
including
AEFIs
attributed
COVID-19
Sweden.
Subjects
were
recruited
from
December
2020
October
2022
stratified
based
on
diagnosis
exposure.
Screening
was
carried
out
two
phases,
multiplex
bead-based
assay
the
first
subset
(until
September
2021)
targeted
assays
for
second
2022).
Positivity
defined
absolute,
relative,
biological/technical
thresholds.
Patients
older
Vaxzevria
vaccine
overrepresented
this
group.
Two
cases
had
antiphospholipid
antibodies
none
PF4
antibodies.
identified
six
positives
protein
S
autoantibodies.
Protein
concentrations
negatively
correlated
autoantibody
response
patients
immunoreactivity
functional
analysis
revealed
low
activity
three
subjects.
Our
reveals
against
which
possibly
underlie
coagulopathic
AEFIs.
Abstract
Three
and
a
half
years
after
the
pandemic
outbreak,
now
that
WHO
has
formally
declared
emergency
is
over,
COVID-19
still
significant
global
issue.
Here,
we
focus
on
recent
developments
in
genetic
genomic
research
COVID-19,
give
an
outlook
state-of-the-art
therapeutical
approaches,
as
gradually
transitioning
to
endemic
situation.
The
sequencing
characterization
of
rare
alleles
different
populations
made
it
possible
identify
numerous
genes
affect
either
susceptibility
or
severity
disease.
These
findings
provide
beginning
new
avenues
pan-ethnic
therapeutic
well
potential
screening
protocols.
causative
virus,
SARS-CoV-2,
spotlight,
but
novel
threatening
virus
could
appear
anywhere
at
any
time.
Therefore,
continued
vigilance
further
warranted.
We
also
note
emphatically
prevent
future
pandemics
other
world-wide
health
crises,
imperative
capitalize
what
have
learnt
from
COVID-19:
specifically,
regarding
its
origins,
world’s
response,
insufficient
preparedness.
This
requires
unprecedented
international
collaboration
timely
data
sharing
for
coordination
effective
response
rapid
implementation
containment
measures.
Rheumatology Science and Practice,
Год журнала:
2024,
Номер
62(1), С. 32 - 54
Опубликована: Фев. 29, 2024
The
pandemic
of
coronavirus
disease
2019
(COVID-19),
etiologically
related
to
the
SARS-CoV-2
virus
(severe
acute
respiratory
syndrome
coronavirus-2),
has
drawn
attention
new
clinical
and
fundamental
problems
in
immunopathology
human
diseases
associated
with
virus-induced
autoimmunity
autoinflammation.
provision
that
“the
experience
gained
rheumatology
process
studying
pathogenetic
mechanisms
pharmacotherapy
immunoinflammatory
rheumatic
as
most
common
severe
forms
autoimmune
autoinflammatory
pathology
humans
will
be
demand
for
deciphering
nature
pathological
processes
underlying
COVID-19
developing
approaches
effective
pharmacotherapy”
was
confirmed
numerous
studies
conducted
over
next
3
years
midst
pandemic.
main
focus
on
a
critical
analysis
data
regarding
role
inflammation,
which
basis
pathogenesis
immune-mediated
context
COVID-19.
Rheumatology Science and Practice,
Год журнала:
2023,
Номер
61(4), С. 397 - 420
Опубликована: Авг. 31, 2023
Two
fundamental
pathologic
processes
are
central
to
the
spectrum
of
chronic
inflammation
mechanisms:
autoimmunity
and
autoinflammation.
Autoimmunity
autoinflammation
mutually
potent
processes;
their
development
is
considered
within
framework
“immunoinflammatory”
continuum,
reflecting
close
relationship
between
innate
acquired
types
immune
response.
leading
mechanism
pathogenesis
a
large
group
inflammatory
human
diseases,
defined
as
autoimmune
frequency
which
in
population
exceeds
10%.
Advances
molecular
biology,
pharmacogenetics
bioinformatics
have
created
prerequisites
for
individualization
therapy
rheumatic
diseases
concept
personalized
medicine.
The
study
immunopathogenesis
mechanisms,
improvement
diagnostics,
deciphering
nature
taxonomy,
approaches
prevention
among
priority
directions
medicine
21st
century.
Molecular Biotechnology,
Год журнала:
2023,
Номер
unknown
Опубликована: Июль 31, 2023
The
effects
of
diabetes
can
be
divided
into
short,
medium
and
long
term
various
human
organ
systems
effected.
present
study
aimed
to
determine
how
much
the
duration
mellitus
(DM)
affect
reparative
ability
body,
immune
response
development
DM
complications.
Interleukin
1-β
(IL-1β)
6
(IL-6)
were
monitored
as
specific
indicators
inflammatory
reaction
C-reactive
protein
(CRP),
leukocyte
count
(WBC)
sedimentation
rate
(ESR)
general
markers
reaction.
Tumour
necrosis
factor
α
(TNF-α)
transforming
growth
β1
(TGF-β1)
observed
polyneuropathy.
All
interleukins
determined
by
ELISA
evaluated
spectrophotometrically.
Michigan
Neuropathy
Screening
Instrument
(MNSI)
is
performed
for
neuropathy
examination.
Patients
with
3
groups,
according
mellitus.
IL-6
levels
correlated
clinical
stage
diabetic
polyneuropathy
at
p
=
0.025
R
0.402;
CRP
0.0001,
0.784
well
correlation
MNSI
score
(R
0.500,
0.034)
in
a
group
patients
lasting
up
10
years.
body
reduced
physiological
age
ages
duration.
weakened
additionally.
dual
activity
cytokines
TGF-β1
long-duration
Diabetes
Mellitus.
Immunobiology,
Год журнала:
2024,
Номер
229(4), С. 152813 - 152813
Опубликована: Май 24, 2024
Post-COVID
symptoms
are
reported
in
10–35
%
of
patients
not
requiring
hospitalization,
and
up
to
80
hospitalized
with
severe
disease.
The
pathogenesis
post-COVID
syndrome
remains
largely
unknown.
Some
evidence
suggests
that
prolonged
inflammation
has
a
key
role
the
most
manifestations.
We
evaluated
panel
inflammatory
immune-mediated
cytokines
individuals
altered
HRCT
features
without
any
long-term
COVID
symptoms.
Blood
samples
89
adult
previously
COVID-19
were
collected
stratified
as
fibrotic
lung
alterations.
Serum
analyte
concentrations
IL-4,
IL-2,
CXCL10
(IP-10),
IL-1β,
TNF-α,
CCL2
(MCP-1),
IL-17A,
IL-6,
IL-10,
IFN-γ,
IL-12p70
TGF-β1
(free
active
form)
quantified
by
bead-based
multiplex
assay.
Clinical
functional
data
recorded
database.
With
use
machine
learning
approach,
IL-32,
IL-8,
IL-10
proved
be
associated
development
sequelae
at
follow-up.
Direct
comparison
cytokine
levels
two
groups
showed
increased
IL-32
decreased
IL-8
impairment.
After
further
stratification
severity
(severe
versus
mild/moderate)
during
emerged
only
showing
patients.
These
findings
contribute
better
understanding
immune
response
potential
prognostic
markers
after
COVID-19.
The
SARS-CoV-2
virus
can
cause
hyperstimulation
of
the
immune
system,
sometimes
leading
to
production
various
autoantibodies
and
increased
levels
interferons
interleukins
in
blood
plasma.
Background/Objectives:
Only
a
few
studies
are
currently
focusing
on
dynamics
immunological
indices
after
any
transferred
infectious
disease
encountered
by
an
organism
for
first
time.
attention
researchers
clinicians
is
captured
antibody
titers
immunologic
markers
(interferons
interleukins),
as
well
correlation
with
changes
symptomatology
long
COVID.
This
paper
discusses
association
antibodies
against
autoantigens
rheumatological
neurological
manifestations
COVID-19.
Our
study
patient
was
36-year-old
man
diagnosed
polyneuropathy,
which
developed
We
conducted
dynamic
follow-up
two
years.
Methods:
plasma
samples
collected
were
analyzed
ELISA
different
autoantigens,
IFN-γ,
variety
interleukins.
Results:
An
between
rheumatologic
neurologic
patients
COVID
symptoms
considered.
Antibody
myelin
basic
protein
(MBP),
double-stranded
DNA
(dsDNA),
single-stranded
IL-1,
IL-6,
IL-10
significantly
during
posthospital
period
when
reported
persistent
COVID,
complaints
decreasing
resolved.
Conclusions:
findings
this
shed
light
alterations
factors,
elucidate
mechanism
infection
disrupts
immunotolerance
eventually
restores
equilibrium,
pathology.
Significantly,
notable
rise
transient
did
not
lead
progression
autoimmune
Journal of Medicinal Chemistry,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 21, 2025
In
addition
to
the
conventional
symptoms
reported
for
COVID-19,
it
is
becoming
increasingly
clear
that
patients
with
long
COVID
are
exhibiting
new
due
emergence
of
autoantibodies
against
G-protein-coupled
receptors,
among
which
human
muscarinic
cholinergic
receptors
(CHRMs)
have
been
prominently
reported.
With
a
chronic
condition
such
as
COVID,
additional
caused
by
anti-CHRM
(AAbs)
proven
be
an
added
burden
on
these
patients.
The
origins
AAbs,
their
interactions
with,
and
effects
function
neural
non-neural
cells
within
nervous
system
remained
unknown.
Furthermore,
specific
symptom
complex
they
contribute
has
not
clearly
understood.
this
context,
we
address
issues
here
suggest
methods
combat
neurological
in
COVID.
Research Square (Research Square),
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 22, 2025
Abstract
In
mammalian
and
human
life,
one
of
the
most
important
problems
is
to
choose
best
defence
against
microorganisms.
Innate
cells
are
good
bacteria,
T
virus
mainly
because
antibody
production
via
helper
B
lymphocytes.
Toll-like
receptor
5
(TLR-5)
a
regulator
this
choice;
when
it
highly
expressed,
inhibited,
innate
favored.
activated
pancreatic
beta
cells,
TLR-5
has
been
found
expressed
may
therefore
be
protected
from
cell
destruction
e.g.,
during
pregnancy.
We
investigated
mRNA
islets
Langerhans
newly
diagnosed
T1D
patients
for
TLR-5.
Also,
we
examined
polymorphisms
between
TLR-5,
metabolic
parameters,
Type
1
Diabetes
(T1D).
was
downregulated
by
one-third
in
compared
controls.
Regarding
polymorphisms,
two
associations
were
monocytes
which
immune
system.
significant
polymorphism
seen
concerning
T1D.
autoimmune
diseases
including
present
study
find
low
values
enhance
cells.
hope
that
findings
mentioned
article
influential
understanding
how
develops.