HMGB1 release by inflammasomes

High-mobility group box 1 (HMGB1) was originally identified as a highly conserved nuclear DNA-binding protein that participates in DNA replication, repair and transcriptional regulation of gene expression. Although the nuclear role of HMGB1 is not quite understood, recent studies characterized the emerging role of extracellular HMGB1 as a prototypical danger signal that regulates inflammatory and repair responses. Under conditions of infection, injury and sterile inflammation, HMGB1 can be passively released from damaged cells or actively secreted from activated immune cells. Inflammasomes, large caspase-1-activating protein complexes, were recently shown to play a critical role in mediating the extracellular release of HMGB1 from activated and infected immune cells.

[1]  M. Lamkanfi.  Emerging inflammasome effector mechanisms , 2011, Nature Reviews Immunology.

[2]  K. Tracey,et al.  Inflammasome-Dependent Release of the Alarmin HMGB1 in Endotoxemia , 2010, The Journal of Immunology.

[3]  V. Dixit,et al.  Manipulation of host cell death pathways during microbial infections. , 2010, Cell host & microbe.

[4]  A. Bowie,et al.  Sensing and Signaling in Antiviral Innate Immunity , 2010, Current Biology.

[5]  G. Núñez,et al.  A Critical Role for Hemolysins and Bacterial Lipoproteins in Staphylococcus aureus-Induced Activation of the Nlrp3 Inflammasome1 , 2009, The Journal of Immunology.

[6]  M. Huang,et al.  NLRP3 (NALP3, Cryopyrin) Facilitates In Vivo Caspase-1 Activation, Necrosis, and HMGB1 Release via Inflammasome-Dependent and -Independent Pathways1 , 2009, The Journal of Immunology.

[7]  V. Dixit,et al.  IL-33 raises alarm. , 2009, Immunity.

[8]  U. Andersson,et al.  High mobility group box chromosomal protein 1 acts as a proliferation signal for activated T lymphocytes. , 2009, Immunobiology.

[9]  S. Akira,et al.  ROLE OF TOLL-LIKE RECEPTORS 2 AND 4, AND THE RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS IN HIGH-MOBILITY GROUP BOX 1-INDUCED INFLAMMATION IN VIVO , 2009, Shock.

[10]  Catherine Rabouille,et al.  Mechanisms of regulated unconventional protein secretion , 2009, Nature Reviews Molecular Cell Biology.

[11]  V. Dixit,et al.  Inflammasomes: guardians of cytosolic sanctity , 2009, Immunological reviews.

[12]  S. Yamada,et al.  Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling. , 2008, Cardiovascular research.

[13]  S. Werner,et al.  Active Caspase-1 Is a Regulator of Unconventional Protein Secretion , 2008, Cell.

[14]  Virginia Pascual,et al.  Dendritic cells and cytokines in human inflammatory and autoimmune diseases. , 2008, Cytokine & growth factor reviews.

[15]  Gabriel Núñez,et al.  Intracellular NOD-like receptors in host defense and disease. , 2007, Immunity.

[16]  M. Bianchi,et al.  High mobility group box 1 protein is released by neural cells upon different stresses and worsens ischemic neurodegeneration in vitro and in vivo , 2007, Journal of neurochemistry.

[17]  K. Tracey,et al.  Systemic inflammation and remote organ injury following trauma require HMGB1. , 2007, American journal of physiology. Regulatory, integrative and comparative physiology.

[18]  L. Audoly,et al.  Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE , 2007, Nature Immunology.

[19]  H. Rauvala,et al.  Analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin) , 2007, Journal of leukocyte biology.

[20]  E. Abraham,et al.  Anti-High-Mobility Group Box Chromosomal Protein 1 Antibodies Improve Survival of Rats with Sepsis , 2006, World Journal of Surgery.

[21]  David C. Lee,et al.  ELEVATED HIGH-MOBILITY GROUP BOX 1 LEVELS IN PATIENTS WITH CEREBRAL AND MYOCARDIAL ISCHEMIA , 2006, Shock.

[22]  V. Dixit,et al.  Cryopyrin activates the inflammasome in response to toxins and ATP , 2006, Nature.

[23]  E. Abraham,et al.  High mobility group box 1 protein interacts with multiple Toll-like receptors. , 2006, American journal of physiology. Cell physiology.

[24]  Peter P. Nawroth,et al.  Release of High Mobility Group Box 1 by Dendritic Cells Controls T Cell Activation via the Receptor for Advanced Glycation End Products1 , 2005, The Journal of Immunology.

[25]  K. Tracey,et al.  The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion , 2005, The Journal of experimental medicine.

[26]  Kevin J. Tracey,et al.  High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal , 2005, Nature Reviews Immunology.

[27]  K. Tracey,et al.  Persistent elevation of high mobility group box-1 protein (HMGB1) in patients with severe sepsis and septic shock* , 2005, Critical care medicine.

[28]  U. Andersson,et al.  RAGE is the Major Receptor for the Proinflammatory Activity of HMGB1 in Rodent Macrophages , 2005, Scandinavian journal of immunology.

[29]  R. Schekman,et al.  Bi-directional protein transport between the ER and Golgi. , 2004, Annual review of cell and developmental biology.

[30]  S. Müller,et al.  HMGB1 is an endogenous immune adjuvant released by necrotic cells , 2004, EMBO reports.

[31]  K. Tracey,et al.  Recombinant HMGB1 with cytokine-stimulating activity. , 2004, Journal of immunological methods.

[32]  K. Tracey,et al.  Extracellular role of HMGB1 in inflammation and sepsis , 2004, Journal of internal medicine.

[33]  E. Abraham,et al.  Involvement of Toll-like Receptors 2 and 4 in Cellular Activation by High Mobility Group Box 1 Protein* , 2004, Journal of Biological Chemistry.

[34]  K. Tracey,et al.  Reversing established sepsis with antagonists of endogenous high-mobility group box 1 , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[35]  A. Parodi,et al.  Quality control and protein folding in the secretory pathway. , 2003, Annual review of cell and developmental biology.

[36]  M. Yamakuchi,et al.  High mobility group box chromosomal protein 1 plays a role in the pathogenesis of rheumatoid arthritis as a novel cytokine. , 2003, Arthritis and rheumatism.

[37]  Jun Yu Li,et al.  High mobility group box chromosomal protein 1: a novel proinflammatory mediator in synovitis. , 2002, Arthritis and rheumatism.

[38]  T. Misteli,et al.  Release of chromatin protein HMGB1 by necrotic cells triggers inflammation , 2002, Nature.

[39]  Michael Bustin,et al.  Regulation of DNA-Dependent Activities by the Functional Motifs of the High-Mobility-Group Chromosomal Proteins , 1999, Molecular and Cellular Biology.

[40]  K. Tracey,et al.  HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.

[41]  A. Aguzzi,et al.  The lack of chromosomal protein Hmg1 does not disrupt cell growth but causes lethal hypoglycaemia in newborn mice , 1999, Nature Genetics.

[42]  D. Shapiro,et al.  HMG-1 stimulates estrogen response element binding by estrogen receptor from stably transfected HeLa cells. , 1999, Molecular endocrinology.

[43]  E. Laue,et al.  Structure of the A-domain of HMG1 and its interaction with DNA as studied by heteronuclear three- and four-dimensional NMR spectroscopy. , 1995, Biochemistry.

[44]  D. Edwards,et al.  Nuclear accessory factors enhance the binding of progesterone receptor to specific target DNA , 1994, The Journal of Steroid Biochemistry and Molecular Biology.

[45]  P. Kraulis,et al.  Structure of the HMG box motif in the B‐domain of HMG1. , 1993, The EMBO journal.

[46]  F. Cozzolino,et al.  A novel secretory pathway for interleukin‐1 beta, a protein lacking a signal sequence. , 1990, The EMBO journal.

[47]  G. Goodwin,et al.  A new group of chromatin-associated proteins with a high content of acidic and basic amino acids. , 1973, European journal of biochemistry.

[48]  J. Tschopp,et al.  The Inflammasomes , 2010, Cell.

[49]  P. Matzinger.  Tolerance, danger, and the extended family. , 1994, Annual review of immunology.