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Diabetes Research Institute, Heinrich-Heine-University, Düsseldorf, Germany
Mammalian 60-kDa heat-shock protein (hsp60) is a key target of T
cell and Ab responses in chronic inflammation or atherosclerosis. We
show in this study that human hsp60 is also an Ag recognized by cells
of the innate immune system, such as macrophages. Both mouse and human
macrophages respond to contact with exogenous human hsp60 with rapid
release of TNF-
; mouse macrophages in addition produce nitric oxide.
The proinflammatory macrophage response is hsp60 dose dependent and
similar in kinetics and extent to LPS stimulation. Human hsp60 was
found to synergize with IFN-
in its proinflammatory activity.
Finally, human hsp60 induces gene expression of the Th1-promoting
cytokines IL-12 and IL-15. These findings identify autologous hsp60 as
a danger signal for the innate immune system, with important
implications for a role of local hsp60 expression/release in chronic
Th1-dependent tissue inflammation.
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