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Human serum IgA downregulates the release of inflammatory cytokines (tumor
necrosis factor-alpha, interleukin-6) in human monocytes
HM Wolf, MB Fischer, H Puhringer, A Samstag, E Vogel and MM Eibl
Institute of Immunology, University of Vienna, Austria.
While the protective effect of IgA antibodies against infection of the
mucosal surfaces is well documented, the mechanisms involved are not
entirely clear. The aim of the current study is to investigate the effect
of human serum IgA on the release of inflammatory cytokines in human
monocytes activated with a particulate stimulus, Haemophilus influenzae
type b (Hib), or soluble lipopolysaccharide (LPS) purified from Escherichia
coli. Our results show that IgA downregulates tumor necrosis factor-alpha
(TNF-alpha) and interleukin-6 (IL-6) production, whereas IgG examined in
parallel had no effect. IgA had no inhibitory effect on Hib-induced
granulocyte-macrophage colony-stimulating factor release. TNF-alpha and
IL-6 release were downmodulated if IgA was present during cytokine
induction, and IgA was also inhibitory if added to Hib-pretreated monocytes
during the phase of cytokine release. These findings indicate that there
are at least two mechanisms whereby IgA antibodies can downregulate
TNF-alpha and IL-6 release in human monocytes: by a mechanism acting during
the time of monocyte activation, and a mechanism that downregulates the
production and/or the release of these cytokines in activated monocytes.
Regulation of TNF-alpha and IL-6 release by IgA may be among the
antiinflammatory mechanisms preventing an uncontrolled release of
potentially noxious levels of inflammatory cytokines during acute and/or
chronic inflammation.
Volume 83,
Issue 5,
pp. 1278-1288,
03/01/1994
Copyright © 1994 by The American Society of Hematology
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