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Objectives:
We studied the role
of the regulatory T
cells CD4+CD25+ (Treg)
and activated
CD4+CD30+ cells in
the pathogenesis of
asthma and their
association with
apoptosis and NF-κB
in patients with
mild intermittent
asthma (MA), severe
persistent asthma
(SA), and healthy
volunteers (HV).
Methods:
Peripheral blood
lymphocytes (PBL)
were extracted from
asthmatic patients
during
exacerbations, and
CD4+ cells were
separated using
Dynal beads.
Immunostaining of
whole PBL for NF-κB,
Bax, and Bcl-2, and
immunostaining of
CD4+ cells for CD25+
and CD30+ cells were
performed using
immunocytochemistry.
Results: Treg
cells were expressed
at higher levels in
MA than in HV and SA
(P<.05), while CD30+
T cells were
expressed at higher
levels in both SA
and MA than in HV
(P<.05), although
there was no
remarkable
difference between
SA and MA (P>.05).
Levels of NF-κB,
Bcl-2, and Bcl-2/Bax
increased, whereas
those of Bax
decreased,
progressively, from
MA to SA (P<.05).
NF-κB levels
correlated directly
with the
Bcl-2/Bax ratio and
with CD4+CD30+ cells
in SA and MA,
whereas CD4+CD30+
cells correlated
inversely with the
Bcl-2/Bax ratio.
Conclusions:
Unregulated Treg
cells probably
return infl ammatory
responses to normal
values during
exacerbations in MA;
however, expression
of Treg cells was
extensively
diminished in SA,
leading to probable
loss of suppressive
control over
underlying immune
reactions. CD4+CD30+
cells were
associated with the
pathogenesis of
asthma but not with
severity. NF-κB
seems to be the
central inflammatory
factor in SA, with a
remarkable loss of
PBL apoptosis,
diminished Treg
levels, and high
CD30+ cell levels
that probably induce
NF-κB, which in turn
blocks the
proapoptotic
potential of CD30
induction itself.
Key words:
Asthma. Apoptosis.
Memory cells.
CD45RO. TH1. TH2.
IL-4. IFN-γ.
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