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The immune system in hypertension.
[severe combined immunodeficiency]
Hypertension
is
generally
attributed
to
perturbations
of
the
vasculature
,
the
kidney
,
and
the
central
nervous
system
.
During
the
past
several
years
,
it
has
become
apparent
that
cells
of
the
innate
and
adaptive
immune
system
also
contribute
to
this
disease
.
Macrophages
and
T
cells
accumulate
in
the
kidneys
and
vasculature
of
humans
and
experimental
animals
with
hypertension
,
and
likely
contribute
to
end-organ
damage
.
We
have
shown
that
mice
lacking
lymphocytes
,
such
as
recombinase-activating
gene
-
deficient
(
RAG-
1
(
-
/
-
)
)
mice
,
have
blunted
hypertension
in
response
to
angiotensin
II
,
increased
salt
levels
,
and
norepinephrine
.
Adoptive
transfer
of
T
cells
restores
the
blood
pressure
response
to
these
stimuli
.
Others
have
shown
that
mice
with
severe
combined
immunodeficiency
have
blunted
hypertension
in
response
to
angiotensin
II
.
Deletion
of
the
RAG
gene
in
Dahl
salt
-sensitive
rats
reduces
the
hypertensive
response
to
salt
feeding
.
The
central
nervous
system
seems
to
orchestrate
immune
cell
activation
.
We
produced
lesions
of
the
anteroventral
third
ventricle
and
showed
that
these
block
T
cell
activation
in
response
to
angiotensin
II
.
Likewise
,
we
showed
that
genetic
manipulation
of
reactive
oxygen
species
in
the
subfornical
organ
modulates
both
hypertension
and
T
cell
activation
.
Current
evidence
indicates
that
production
of
cytokines
including
tumor
necrosis
factor
alpha
,
interleukin
17
,
and
interleukin
6
contribute
to
hypertension
,
likely
by
promoting
vasoconstriction
,
production
of
reactive
oxygen
species
,
and
sodium
reabsorption
in
the
kidney
.
We
propose
a
working
hypothesis
linking
the
sympathetic
nervous
system
,
immune
cells
,
the
production
of
cytokines
,
and
ultimately
vascular
and
renal
dysfunction
,
leading
to
augmentation
of
hypertension
.
Diseases
Validation
Diseases presenting
"factor alpha"
symptom
epidermolysis bullosa simplex
inclusion body myositis
severe combined immunodeficiency
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