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Differential Deactivation of Human Dendritic Cells by Endotoxin
Desensitization: Role of Tumor Necrosis Factor- and Prostaglandin E2
Claudia Rieser,
Christine Papesh,
Manfred Herold,
Günther Böck,
Reinhold Ramoner,
Helmut Klocker,
Georg Bartsch, and
Martin Thurnher
From the Departments of Urology and Internal Medicine; and the
Institute of General and Experimental Pathology, University of
Innsbruck, A-6020 Innsbruck, Austria
The endotoxin (lipopolysaccharide)-induced cytokine response is
followed by a state of unresponsiveness to lipopolysaccharide (LPS)
referred to as LPS tolerance or endotoxin desensitization. LPS
tolerance, which can be experimentally induced in vitro and in vivo, is
also known to occur in septic disease. Here, we evaluated whether
dendritic cells (DC), the most potent antigen-presenting cells, are
also subject to this phenomenon. Single doses of LPS added at the
initiation of DC culture inhibited in a dose-dependent fashion the
production of tumor necrosis factor- (TNF-), interleukin-10 (IL-10), and IL-12, but not the production of IL-8, in response to a
second LPS challenge in day-5 DC. In addition, the LPS-induced expression of the CD83 maturation antigen was inhibited in these cells.
Moreover, the endocytic activity of DC generated in the presence of LPS
was dramatically reduced. DC desensitized with LPS were potent
stimulators of T-cell proliferation but poor inducers of interferon-
(IFN-) production in the allogeneic mixed leukocyte reaction.
TNF- and prostaglandin E2, two major products of LPS stimulation,
could replace LPS for the induction of tolerance to LPS. Moreover,
treatment of desensitized DC with TNF- plus prostaglandin E2 fully
restored CD83 expression and partially restored IL-12 production as
well as the IFN--inducing activity of DC in the mixed leukocyte
reaction. Our data show that human DC are highly susceptible to the
induction of LPS tolerance, which seems to be a state of differential
deactivation in which some functions are impaired whereas others are
retained. Tolerization at the level of the professional
antigen-presenting cell by inflammatory mediators may play an important
role in septic disease and in the origin of cancers associated with
chronic inflammation.
Blood, Vol. 91 No. 9 (May 1), 1998:
pp. 3112-3117
© 1998 by The American Society of Hematology.
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