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Membrane microdomain organization, calcium signal, and NFAT activation as an important axis in polarized Th cell function.
[gm1 gangliosidosis]
T
helper
lymphocytes
become
polarized
upon
antigen
and
cytokine
stimuli
received
after
their
maturation
in
the
thymus
.
Since
the
balance
of
Th
1
and
Th
2
responses
is
critical
in
healthy
and
pathological
immune
responses
,
understanding
the
molecular
base
of
T
cell
polarization
still
remained
an
important
question
.
Using
our
Th
0
/
Th
1
/
Th
2
hybridoma
model
system
,
we
performed
a
comparative
study
on
polarized
Th
1
and
Th
2
cells
in
terms
of
their
membrane
raft
expression
/
composition
,
their
TCR
mediated
activation
signaling
,
and
sensitivity
to
activation-induced
cell
death
(
AICD
)
using
flow
and
image
cytometric
methods
.
We
show
here
that
the
TCR
stimulation
induced
more
intense
and
sustained
Ca
(
2
+
)
-
response
in
Th
1
cells
compared
to
Th
2
ones
correlates
well
with
a
shorter
nuclear
residence
time
of
the
Ca
(
2
+
)
-
dependent
NFAT
transcription
factor
in
Th
2
cells
.
In
addition
,
NFAT
translocation
directly
depended
on
lipid
raft
integrity
/
membrane
cholesterol
level
.
Expression
pattern
of
raftophilic
accessory
proteins
(
CD
4
,
CD
59
,
and
CD
48
)
and
lipids
(
GM
1
,
cholesterol
)
were
also
different
in
the
Th
1
and
Th
2
hybridomas
,
similarly
to
differentiated
spleen
Th
cells
.
The
activation-induced
,
remarkably
clustered
and
polarized
membrane
distribution
of
TCR
/
CD
3
complex
in
Th
1
,
but
not
in
Th
2
cells
,
together
with
an
increased
raft
localization
of
Kv
1
.
3
ion
channels
regulating
the
Ca
(
2
+
)
-
response
,
are
consistent
with
the
above
properties
of
NFAT
.
Finally
,
the
polarized
Th
cells
,
especially
Th
1
,
were
more
sensitive
to
AICD
than
their
unpolarized
Th
0
precursor
.
These
results
suggest
that
the
membrane
microdomain
organization-
Ca
(
2
+
)
-
signaling-
NFAT
activation
axis
is
an
important
determinant
of
polarized
Th
cell
effector
function
and
fate
.
Diseases
Validation
Diseases presenting
"raftophilic accessory proteins"
symptom
gm1 gangliosidosis
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