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High Mobility Group B1 Protein Suppresses the Human Plasmacytoid Dendritic Cell Response to TLR9 Agonists

Petar J. Popovic, Richard DeMarco, Michael T. Lotze, Steven E. Winikoff, David L. Bartlett, Arthur M. Krieg, Z. Sheng Guo, Charles K. Brown, Kevin J. Tracey and Herbert J. Zeh III
J Immunol December 15, 2006, 177 (12) 8701-8707; DOI: https://doi.org/10.4049/jimmunol.177.12.8701
Petar J. Popovic
*Division of Surgical Oncology and
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Richard DeMarco
*Division of Surgical Oncology and
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Michael T. Lotze
†Translational Research, Department of Surgery and Molecular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15232;
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Steven E. Winikoff
*Division of Surgical Oncology and
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David L. Bartlett
*Division of Surgical Oncology and
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Arthur M. Krieg
‡Coley Pharmaceutical Group, Wellesley, MA 02481; and
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Z. Sheng Guo
*Division of Surgical Oncology and
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Charles K. Brown
*Division of Surgical Oncology and
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Kevin J. Tracey
§Institute for Medical Research, North Shore-Long Island Jewish Research Institute, Manhasset, NY 11030
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Herbert J. Zeh III
*Division of Surgical Oncology and
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Abstract

Plasmacytoid dendritic cells (PDC) are innate immune effector cells that are recruited to sites of chronic inflammation, where they modify the quality and nature of the adaptive immune response. PDCs modulate adaptive immunity in response to signals delivered within the local inflammatory milieu by pathogen- or damage-associated molecular pattern, molecules, and activated immune cells (including NK, T, and myeloid dendritic cells). High mobility group B1 (HMGB1) is a recently identified damage-associated molecular pattern that is released during necrotic cell death and also secreted from activated macrophages, NK cells, and mature myeloid dendritic cells. We have investigated the effect of HMGB1 on the function of PDCs. In this study, we demonstrate that HMGB1 suppresses PDC cytokine secretion and maturation in response to TLR9 agonists including the hypomethylated oligodeoxynucleotide CpG- and DNA-containing viruses. HMGB1-inhibited secretion of several proinflammatory cytokines including IFN-α, IL-6, TNF-α, inducible protein-10, and IL-12. In addition, HMGB1 prevented the CpG induced up-regulation of costimulatory molecules on the surface of PDC and potently suppressed their ability to drive generation of IFN-γ-secreting T cells. Our observations suggest that HMGB1 may play a critical role in regulating the immune response during chronic inflammation and tissue damage through modulation of PDC function.

  • Received October 20, 2005.
  • Accepted September 29, 2006.
  • Copyright © 2006 by The American Association of Immunologists
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The Journal of Immunology: 177 (12)
The Journal of Immunology
Vol. 177, Issue 12
15 Dec 2006
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High Mobility Group B1 Protein Suppresses the Human Plasmacytoid Dendritic Cell Response to TLR9 Agonists
Petar J. Popovic, Richard DeMarco, Michael T. Lotze, Steven E. Winikoff, David L. Bartlett, Arthur M. Krieg, Z. Sheng Guo, Charles K. Brown, Kevin J. Tracey, Herbert J. Zeh
The Journal of Immunology December 15, 2006, 177 (12) 8701-8707; DOI: 10.4049/jimmunol.177.12.8701

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High Mobility Group B1 Protein Suppresses the Human Plasmacytoid Dendritic Cell Response to TLR9 Agonists
Petar J. Popovic, Richard DeMarco, Michael T. Lotze, Steven E. Winikoff, David L. Bartlett, Arthur M. Krieg, Z. Sheng Guo, Charles K. Brown, Kevin J. Tracey, Herbert J. Zeh
The Journal of Immunology December 15, 2006, 177 (12) 8701-8707; DOI: 10.4049/jimmunol.177.12.8701
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