CCL19/MIP-3β as a key mediator in the production of anti-GPIIb/IIIa antibody-producing B cells in patients with chronic hepatitis C
J Iida,
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Haruki Uojima,
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Takashi Satoh
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et al.
Cytokine,
Journal Year:
2025,
Volume and Issue:
190, P. 156915 - 156915
Published: March 19, 2025
Language: Английский
Research and Advances on Langerhans Cell Histiocytosis-Related Liver Injury
丽莉 张
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Advances in Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
15(04), P. 2650 - 2657
Published: Jan. 1, 2025
Language: Английский
HLA-F expression on CD4 T cells in HIV-1 is linked to the presence of viremia and modulated by KIR3DS1
Angelique Hœlzemer,
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Timo Trenkner,
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Sébastien Brias
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et al.
Research Square (Research Square),
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 25, 2025
Abstract
KIR3DS1
is
an
activating
natural
killer
(NK)
cell
receptor
gene–
present
in
10-40%
of
humans–
and
associated
with
extended
AIDS-free
survival.
Although
its
ligand
HLA-F
has
been
identified,
the
underlying
protective
mechanism
HIV-1
not
yet
understood.
We
sought
to
uncover
role
KIR3DS1/HLA-F
axis
through
investigating
surface
transcriptional
changes
during
acute
chronic
infection.
HLA-F
+
CD4
T
cells
were
detected
people
living
HIV
(PLHIV)
without
antiretroviral
treatment
(N=102)
frequencies
correlated
viremia
but
count.
Single-cell
transcriptome
analyses
PLHIV
following
acquisition
revealed
increased
mRNA
levels
innate
signaling
signatures.
In
vitro,
was
upregulated
both
HIV-1–infected
bystander
cells.
Functional
studies
demonstrated
that
bystander-activated
reduced
presence
NK
infection,
depleting
frequency
Genotyping
our
cohort
KIR3DS1+
exhibited
significantly
lower
Taken
together,
these
results
establish
as
a
novel
marker
activation
linked
suggest
immunoregulatory
controlling
HIV-1-mediated
inflammation
by
killing
activated
Language: Английский
The Impact of Liver Steatosis on Interleukin and Growth Factors Kinetics during Chronic Hepatitis C Treatment
Journal of Clinical Medicine,
Journal Year:
2024,
Volume and Issue:
13(16), P. 4849 - 4849
Published: Aug. 16, 2024
Background/Objectives:
Various
biological
response
modifiers
play
important
roles
in
the
immunopathogenesis
of
chronic
hepatitis
C
(CHC).
While
serum
levels
cytokines
and
growth
factors
change
with
disease
severity
treatment
responses,
impact
concomitant
liver
steatosis
on
systemic
inflammatory
is
largely
unknown.
The
aim
this
study
was
to
analyze
characteristics
kinetics
profiles
interleukins
CHC
patients
steatotic
(SLD).
Methods:
Serum
concentrations
12
(IL-5,
IL-13,
IL-2,
IL-6,
IL-9,
IL-10,
IFN-γ,
TNF-α,
IL-17A,
IL-17F,
IL-4
IL-22)
6
(Angiopoietin-2,
EGF,
EPO,
HGF,
SCF,
VEGF)
were
analyzed
56
at
four
time
points
(baseline,
week
4,
8
SVR12)
bead-based
flow
cytometry
assay.
Results:
At
baseline,
SLD
had
significantly
lower
IL-13
IL-22
higher
VEGF
ANG.
In
a
subgroup
advanced
fibrosis,
linked
IL-4,
IL-5,
HGH
VEGF.
Distinct
cytokine
during
DAA
observed,
identified
as
main
source
variation
for
IL-22,
Patients
SVR12
HGF
concentrations.
Conclusions:
associated
distinct
factor
treatment,
which
might
be
capacity
regeneration
contribute
fibrosis
persistence.
Language: Английский