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Do the placental barrier, parasite genotype and Toll-like receptor polymorphisms contribute to the course of primary infection with various Toxoplasma gondii genotypes in pregnant women?
[congenital toxoplasmosis]
Toxoplasma
gondii
has
a
highly
clonal
genetic
structure
classified
into
three
major
genetic
types
,
I
,
II
,
and
III
,
plus
additional
recombinant
and
atypical
strains
.
In
humans
,
type
I
and
atypical
strains
usually
associate
with
severe
toxoplasmosis
.
Type
II
strains
,
predominantly
identified
in
European
countries
and
the
United
States
,
correlate
with
a
differential
course
of
toxoplasmosis
.
During
pregnancy
,
the
important
protective
role
of
the
placenta
against
maternal
-
fetal
T
.
gondii
transmission
has
been
reported
.
T
.
gondii
preferentially
colonizes
extravillous
trophoblasts
as
compared
to
syncytiotrophoblasts
.
The
latter
compartment
was
suggested
to
act
as
the
real
barrier
to
the
fetal
dissemination
of
T
.
gondii
.
Alterations
in
immune
response
to
particular
T
.
gondii
strains
were
observed
.
Higher
transcription
levels
of
IP-
10
,
IL
-
1
β
,
IL
-
6
,
IL
-
10
,
IL
-
12
cytokines
,
and
NF-κB
translocation
to
the
nucleus
were
more
often
documented
for
type
II
strains
than
type
I
strains
.
Since
the
induction
of
IL
-
12
during
type
II
infection
was
Myd
88
-
dependent
,
the
involvement
of
Toll-like
receptors
(
TLRs
)
in
the
immunity
against
these
strains
was
suggested
.
Differential
expression
of
TLRs
depends
on
placental
cell
types
and
gestational
age
.
The
expression
of
TLR
2
and
TLR
4
in
the
first
trimester
of
pregnancy
was
reported
only
for
villous
cytotrophoblasts
and
extravillous
trophoblasts
,
but
not
for
syncytiotrophoblasts
.
The
involvement
of
single
-nucleotide
polymorphisms
(
SNPs
)
in
the
TLR
genes
in
infectious
pathogenicity
,
including
toxoplasmic
retinochoroiditis
,
points
at
a
possible
involvement
of
TLR
alterations
in
immunity
against
T
.
gondii
.
We
conclude
that
studies
on
TLR
contributions
in
the
maternal
-
fetal
transmission
of
particular
parasite
strains
and
congenital
toxoplasmosis
are
warranted
.
Diseases
Validation
Diseases presenting
"highly clonal"
symptom
congenital toxoplasmosis
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