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Open Access Green as soon as Postprint is submitted to ZB.
Different natural killer (NK) receptor expression and immunoglobulin E (IgE) regulation by NK1 and NK2 cells.
Clin. Exp. Immunol. 140, 301-309 (2005)
Many studies concerning the role of T cells and cytokines in allergy have been
performed, but little is known about the role of natural killer (NK) cells.
Accordingly, the expression of co-stimulatory, inhibitory and apoptosis receptors,
cytokine profiles and their effect on immunoglobulin isotypes were
investigated in polyallergic atopic dermatitis (AD) patients with hyper immunoglobulin
E (IgE) and healthy individuals. AD patients showed significantly
decreased peripheral blood NK cells compared to healthy individuals. Freshly
isolated NK cells of polyallergic patients spontaneously released higher
amounts of interleukin (IL)-4, IL-5, IL-13 and interferon (IFN)-g
compared to
healthy individuals. NK cells were differentiated to NK1 cells by IL-12 and
neutralizing anti-IL-4 monoclonal antibodies (mAb), and to NK2 cells by IL-
4 and neutralizing anti-IL-12 mAb. Following IL-12 stimulation, NK cells produced
increased levels of IFN-g
and decreased IL-4. In contrast, stimulation of
NK cells with IL-4 inhibited IFN-g
, but increased IL-13, production. The effect
of NK cell subsets on IgE regulation was examined in co-cultures of
in vitro
differentiated NK cells with peripheral blood mononuclear cells (PBMC) or
B cells. NK1 cells significantly inhibited IL-4- and soluble CD40-ligandstimulated
IgE production; however, NK2 cells did not have any effect. The
inhibitory effect of NK1 cells on IgE production was blocked by neutralization
of IFN-g
. Except for CD40, NK cell subsets showed different expression of
killer-inhibitory receptors and co-stimulatory molecules between the polyallergic
and healthy subjects. These results indicate that human NK cells show
differences in numbers, su
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
allergy; IgE; IgG4; KIR receptors; natural killer cells
ISSN (print) / ISBN
0009-9104
e-ISSN
1365-2249
Quellenangaben
Volume: 140,
Pages: 301-309
Publisher
Wiley
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Molecular Immunology (IMI)