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Blood, 15 May 2002, Vol. 99, No. 10, pp. 3676-3682
IMMUNOBIOLOGY
Human platelets express heat shock protein receptors and regulate
dendritic cell maturation
Norbert Hilf,
Harpreet Singh-Jasuja,
Petra Schwarzmaier,
Cécile Gouttefangeas,
Hans-Georg Rammensee, and
Hansjörg Schild
From the Department of Immunology, University of
Tübingen, Germany.
Immunizations using the endoplasmic reticulum-resident heat shock
protein Gp96 induce specific immune responses. Specificity is based on
the major histocompatibility complex class I-restricted cross-presentation of Gp96-associated peptides derived from endogenous proteins. Initiation of the immune response depends on the ability of
Gp96 to induce the production of proinflammatory cytokines by
macrophages and dendritic cells (DCs) and of their maturation in a
fashion presumably independent of associated peptide. Both events are
mediated by Gp96 receptors on antigen-presenting cells. It is known
that Gp96 is released from cells at necrosis induced, for example, by
virus infection. Although this event supports the efficient induction
of immune responses, it might also interfere with processes that are
susceptible to chronic inflammation, such as wound healing after tissue
damage. Therefore, Gp96-mediated stimulation of the immune system
requires tight regulation. Here we show that human thrombocytes
specifically interact with Gp96 and that binding of Gp96 to platelets
is enhanced more than 10-fold on activation by thrombin. Gp96
interferes with neither thrombin-induced platelet activation nor
platelet aggregation. However, the presence of platelets during
Gp96-mediated DC activation reduces the secretion of proinflammatory
cytokines and the activation of DCs. This effect is independent of
soluble platelet factors and cell-to-cell contact between DCs and
thrombocytes. Thus, we provide evidence for a regulatory mechanism that
neutralizes Gp96 molecules systemically, especially in the blood. This
effect might be of significance in wounds in which chronic inflammation
and immune responses against autoantigens have to be prevented.
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