JAMA Neurology,
Journal Year:
2021,
Volume and Issue:
78(11), P. 1333 - 1333
Published: Sept. 20, 2021
Overall,
immunotherapy
has
been
shown
to
improve
outcomes
and
reduce
relapses
in
individuals
with
N-methyl-d-aspartate
receptor
(NMDAR)
antibody
encephalitis
(NMDARE);
however,
the
superiority
of
specific
treatments
combinations
remains
unclear.To
map
use
safety
immunotherapies
NMDARE,
identify
early
predictors
poor
functional
outcome
relapse,
evaluate
changes
disease
over
14
years
since
first
reports
assess
Anti-NMDAR
Encephalitis
One-Year
Functional
Status
(NEOS)
score.Systematic
search
PubMed
from
inception
January
1,
2019.Published
articles
including
patients
NMDARE
positive
NMDAR
antibodies
available
individual
data.Individual
patient
data
on
immunotherapies,
clinical
characteristics
at
presentation,
course,
final
(modified
Rankin
Scale
[mRS]
score)
were
entered
into
multivariable
logistic
regression
models.The
planned
study
12
months
onset
(good,
mRS
score
0
2;
poor,
greater
than
2)
monophasic
course
(absence
relapse
24
or
later
onset).Data
1550
652
evaluated.
Of
these,
1105
1508
(73.3%)
female
707
1526
(46.3%)
18
younger
onset.
Factors
event
that
significantly
associated
good
included
adolescent
age
first-line
treatment
therapeutic
apheresis,
corticosteroids
plus
intravenous
immunoglobulin
(IVIG),
IVIG
apheresis.
2
65
older
onset,
intensive
care
unit
admission,
extreme
delta
brush
pattern
electroencephalography,
lack
within
30
days
maintenance
for
6
more.
nonrelapsing
rituximab
Adolescent
was
relapsing
disease.
Rituximab
increased
13.5%
(52
384;
2007
2013)
28.3%
(311
1100;
2013
2019)
(P
<
.001),
concurrent
a
falling
rate
same
period
(22%
[12
55]
2008
earlier;
10.9%
[35
322]
2017
later;
P
=
.006).
Modified
NEOS
(including
4
5
original
items)
probability
status
1
year
(20.1%
[40
199]
points;
43.8%
[77
176]
3
.05).Factors
influencing
are
different
need
be
considered
independently
development
evidence-based
optimal
management
guidelines
NMDARE.
Science,
Journal Year:
2022,
Volume and Issue:
375(6578), P. 296 - 301
Published: Jan. 14, 2022
Multiple
sclerosis
(MS)
is
a
chronic
inflammatory
demyelinating
disease
of
the
central
nervous
system
unknown
etiology.
We
tested
hypothesis
that
MS
caused
by
Epstein-Barr
virus
(EBV)
in
cohort
comprising
more
than
10
million
young
adults
on
active
duty
US
military,
955
whom
were
diagnosed
with
during
their
period
service.
Risk
increased
32-fold
after
infection
EBV
but
was
not
other
viruses,
including
similarly
transmitted
cytomegalovirus.
Serum
levels
neurofilament
light
chain,
biomarker
neuroaxonal
degeneration,
only
seroconversion.
These
findings
cannot
be
explained
any
known
risk
factor
for
and
suggest
as
leading
cause
MS.
Frontiers in Immunology,
Journal Year:
2020,
Volume and Issue:
11
Published: Dec. 10, 2020
The
human
microbiota
has
a
fundamental
role
in
host
physiology
and
pathology.
Gut
microbial
alteration,
also
known
as
dysbiosis,
is
condition
associated
not
only
with
gastrointestinal
disorders
but
diseases
affecting
other
distal
organs.
Recently
it
became
evident
that
the
intestinal
bacteria
can
affect
central
nervous
system
(CNS)
inflammation.
tract
are
communicating
through
bidirectional
network
of
signaling
pathways
called
gut-brain
axis,
which
consists
multiple
connections,
including
vagus
nerve,
immune
system,
bacterial
metabolites
products.
During
these
dysregulated
altered
permeability
blood-brain
barrier
(BBB)
neuroinflammation.
However,
numerous
mechanisms
behind
impact
gut
neuro-development
-pathogenesis
remain
poorly
understood.
There
several
involved
CNS
homeostasis
Among
those,
inflammasome
pathway
been
linked
to
neuroinflammatory
conditions
such
sclerosis,
Alzheimer’s
Parkinson’s
diseases,
anxiety
depressive-like
disorders.
complex
assembles
upon
cell
activation
due
exposure
microbes,
danger
signals,
or
stress
lead
production
pro-inflammatory
cytokines
(interleukin-1β
interleukin-18)
pyroptosis.
Evidences
suggest
there
reciprocal
influence
brain.
how
this
precisely
working
yet
be
discovered.
Herein,
we
discuss
status
knowledge
open
questions
field
focusing
on
function
products
cells
during
healthy
inflammatory
conditions,
neuropsychiatric
In
particular,
focus
innate
mechanism
certain
microbes.
Cell,
Journal Year:
2018,
Volume and Issue:
175(1), P. 85 - 100.e23
Published: Aug. 30, 2018
Multiple
sclerosis
is
an
autoimmune
disease
that
caused
by
the
interplay
of
genetic,
particularly
HLA-DR15
haplotype,
and
environmental
risk
factors.
How
these
etiologic
factors
contribute
to
generating
autoreactive
CD4+
T
cell
repertoire
not
clear.
Here,
we
demonstrate
self-reactivity,
defined
as
"autoproliferation"
peripheral
Th1
cells,
elevated
in
patients
carrying
haplotype.
Autoproliferation
mediated
memory
B
cells
a
HLA-DR-dependent
manner.
Depletion
vitro
therapeutically
vivo
anti-CD20
effectively
reduces
autoproliferation.
receptor
deep
sequencing
showed
autoproliferating
are
enriched
for
brain-homing
cells.
Using
unbiased
epitope
discovery
approach,
identified
RASGRP2
target
autoantigen
expressed
brain
These
findings
will
be
instrumental
address
important
questions
regarding
pathogenic
B-T
interactions
multiple
possibly
also
develop
novel
therapies.
