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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 218-223
Impaired antigen presentation by human monocytes during endotoxin
tolerance
Kerstin Wolk,
Wolf-Dietrich Döcke,
Volker von Baehr,
Hans-Dieter Volk, and
Robert Sabat
From the Institute of Medical Immunology, Medical School
Charité, Humboldt University, Berlin, Germany
Endotoxin tolerance (ET) has been described as a temporary
alteration in the lipopolysaccharide (LPS) response of monocytic cells
after an initial LPS exposure with respect to the production of soluble
immunomodulators. Apart from the LPS response, monocytic cells play an
important role in initiation of the specific immune response as
antigen-presenting cells. This study investigated the capacity of human
blood monocytes to induce T-cell stimulation in ET. First, the
expression of monocyte surface molecules, important for T-cell
interaction, was analyzed by flow cytometry. In vitro priming of
peripheral blood mononuclear cells with LPS clearly down-regulates
major histocompatibility complex class II molecules and the
costimulatory molecule CD86. Both changes were dependent on the
endogenous interleukin (IL)-10 and less so on the transforming growth
factor- . In contrast, other accessory molecules on monocytes were
only marginally down-regulated (CD58), were not significantly changed
during ET (CD40), or even remained up-regulated after initial LPS
priming (CD54, CD80). Second, an impact of these phenotypic alterations
on the accessory function of monocytes was observed. This was
manifested as diminished T-cell proliferation and interferon (IFN)-
release in response to the presence of different recall antigens.
Neutralizing IL-10 during LPS priming prevented the diminished T-cell
IFN- production but had little effect on T-cell proliferation. These
data confirm that ET is an appropriate model of the monocyte functional
state in immunoparalysis, which is frequently observed in patients
after septic shock, trauma, or major surgery.
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