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Exogenous Heat Shock Protein gp96 Ameliorates CD4+CD62L+ T-Cell-mediated Transfer Colitis.
[severe combined immunodeficiency]
The
heat
shock
protein
gp
96
is
an
endoplasmic
reticulum
chaperone
involved
in
endoplasmic
reticulum
stress
reactions
.
gp
96
binds
antigens
and
is
secreted
into
extracellular
space
on
cell
stress
.
After
reinternalization
by
antigen
presenting
cells
,
antigens
can
be
transferred
to
major
histocompatibility
complex
molecules
.
In
recent
studies
,
we
found
induction
of
gp
96
during
differentiation
of
intestinal
macrophages
,
whereas
it
was
absent
in
intestinal
macrophages
of
patients
with
Crohn
's
disease
.
To
study
immuno-modulating
effects
of
gp
96
in
T
-
cell
transfer
colitis
BALB
/
c
donor
mice
were
injected
with
2
×
100
μg
gp
96
.
After
1
week
,
2
.
5
×
10
CD
4
CD
6
2
L
cells
were
isolated
from
spleens
and
injected
into
severe
combined
immunodeficiency
recipients
.
Another
group
received
cells
from
untreated
donors
and
was
treated
with
100
μg
gp
96
after
transfer
.
Control
groups
received
cells
from
untreated
donors
,
or
buffer
alone
.
After
transfer
of
CD
4
CD
6
2
L
T
cells
from
gp
96
-
pretreated
donors
,
mice
(
TBT
gp
96
)
showed
an
initial
weight
loss
,
but
after
3
weeks
,
they
recovered
and
reached
the
starting
weight
after
5
weeks
.
Mice
treated
with
gp
96
after
transfer
(
TAT
gp
96
)
showed
a
delayed
weight
loss
in
comparison
with
the
CD
4
CD
6
2
L
group
.
The
histological
scores
in
CD
4
CD
6
2
L
mice
were
2
.
6
±
0
.
1
,
in
TBT
gp
96
mice
1
.
3
±
0
.
3
(
CD
4
CD
6
2
L
versus
TBT
gp
96
:
P
<
0
.
05
)
and
in
mice
treated
after
transfer
1
.
9
±
0
.
1
(
CD
4
CD
6
2
L
versus
TAT
gp
96
:
P
<
0
.
05
)
.
These
findings
indicate
an
essential
role
of
gp
96
in
the
maintenance
of
tolerance
against
luminal
antigens
in
the
intestinal
mucosa
.
The
absence
of
gp
96
in
intestinal
macrophages
of
patients
with
Crohn
's
disease
might
provoke
loss
of
this
tolerance
mediating
mechanism
.
Diseases
Validation
Diseases presenting
"delayed weight loss in comparison with the cd4cd62l"
symptom
severe combined immunodeficiency
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