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Institut für Klinische Mikrobiologie, Immunologie und Hygiene der Friedrich-Alexander Universität Erlangen-Nürnberg, Erlangen, Germany
Dendritic cells (DC) are unique in their ability to initiate a
primary immune response by the presentation of soluble Ags to T cells.
Recent studies have shown that DC also phagocytose particulate Ags
including the intracellular pathogen Mycobacterium
tuberculosis. However, it is not known whether DC contain the
growth of intracellular organisms or allow unlimited replication. To
address this question, we infected human DC with a virulent strain of
M. tuberculosis and monitored the intracellular growth.
The bacteria grew two orders of magnitude within 7 days of culture.
Among cytokines known to modulate mycobacterial growth particularly in
murine macrophages (TNF-
, IFN-
, TGF-ß, IL-4), only IL-10
modulated the growth in human DC. This effect was specific for immature
dendritic cells, as IL-10 did not induce growth inhibition in human
macrophages. In searching for the mechanism of growth inhibition, we
found that IL-10 induces the down-regulation of the DC marker CD1,
while the macrophage marker CD14 was up-regulated. Functionally,
IL-10-treated cells had a reduced capacity to induce an alloresponse,
but phagocytic uptake of M. tuberculosis was more
efficient. We also show that DC are inferior to macrophages in
containing mycobacterial growth. These findings show that IL-10
converts DC into macrophage-like cells, thereby inducing the growth
inhibition of an intracellular pathogen. At the site of a local immune
response, such as a tuberculous granuloma, IL-10 might therefore
participate in the composition of the cellular microenvironment by
affecting the maturity and function of DC.
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