High-mobility group box 1 protein (HMGB1) neutralization ameliorates experimental autoimmune encephalomyelitis.

[1]  K. Tracey,et al.  Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release , 2012, The Journal of experimental medicine.

[2]  M. Schachner,et al.  HMGB1 in Development and Diseases of the Central Nervous System , 2012, Molecular Neurobiology.

[3]  L. Varani,et al.  HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4 , 2012, The Journal of experimental medicine.

[4]  Aaron J. Martin,et al.  Tolerance Induced by Apoptotic Antigen-Coupled Leukocytes Is Induced by PD-L1+ and IL-10–Producing Splenic Macrophages and Maintained by T Regulatory Cells , 2011, The Journal of Immunology.

[5]  U. Andersson,et al.  Monoclonal Anti-HMGB1 (High Mobility Group Box Chromosomal Protein 1) Antibody Protection in Two Experimental Arthritis Models , 2011, Molecular medicine.

[6]  K. Tracey,et al.  HMGB1 is a therapeutic target for sterile inflammation and infection. , 2011, Annual review of immunology.

[7]  Q. Gong,et al.  Neutralization of the extracellular HMGB1 released by ischaemic damaged renal cells protects against renal ischaemia-reperfusion injury. , 2011, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

[8]  I. Maruyama,et al.  High Mobility Group Box 1 Is Upregulated After Spinal Cord Injury and Is Associated With Neuronal Cell Apoptosis , 2010, Spine.

[9]  David M. Wilson,et al.  Stoichiometry of Base Excision Repair Proteins Correlates with Increased Somatic CAG Instability in Striatum over Cerebellum in Huntington's Disease Transgenic Mice , 2009, PLoS genetics.

[10]  M. Bianchi,et al.  HMGB1 loves company , 2009, Journal of leukocyte biology.

[11]  S. Miller,et al.  Molecular mechanisms of T‐cell receptor and costimulatory molecule ligation/blockade in autoimmune disease therapy , 2009, Immunological reviews.

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

[13]  Yang Liu,et al.  CD24 and Siglec-10 Selectively Repress Tissue Damage–Induced Immune Responses , 2009, Science.

[14]  M. Bianchi,et al.  Induction of inflammatory and immune responses by HMGB1–nucleosome complexes: implications for the pathogenesis of SLE , 2008, The Journal of experimental medicine.

[15]  H. Lassmann,et al.  Pivotal Advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis , 2008, Journal of leukocyte biology.

[16]  Lieping Chen,et al.  PD‐1 ligands expressed on myeloid‐derived APC in the CNS regulate T‐cell responses in EAE , 2008, European journal of immunology.

[17]  J. She,et al.  Extracellular High-Mobility Group Box 1 Acts as an Innate Immune Mediator to Enhance Autoimmune Progression and Diabetes Onset in NOD Mice , 2008, Diabetes.

[18]  D. Green,et al.  Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein. , 2008, Immunity.

[19]  B. Funke,et al.  High-Mobility Group Box-1 in Ischemia-Reperfusion Injury of the Heart , 2008, Circulation.

[20]  Jung‐Bin Kim,et al.  Induction and subcellular localization of high‐mobility group box–1 (HMGB1) in the postischemic rat brain , 2008, Journal of neuroscience research.

[21]  M. Bianchi,et al.  High‐mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity , 2007, Immunological reviews.

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

[23]  S. Miller,et al.  CNS myeloid DCs presenting endogenous myelin peptides 'preferentially' polarize CD4+ TH-17 cells in relapsing EAE , 2007, Nature Immunology.

[24]  C. Bendotti,et al.  Distribution and cellular localization of high mobility group box protein 1 (HMGB1) in the spinal cord of a transgenic mouse model of ALS , 2007, Neuroscience Letters.

[25]  H. Rauvala,et al.  Pivotal advance: analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin). , 2007, Journal of leukocyte biology.

[26]  Jong-sang Park,et al.  HMGB1, a Novel Cytokine-Like Mediator Linking Acute Neuronal Death and Delayed Neuroinflammation in the Postischemic Brain , 2006, The Journal of Neuroscience.

[27]  K. Tracey,et al.  Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock , 2006, Molecular medicine.

[28]  M. Lotze,et al.  Hepatic Ischemia/Reperfusion Injury Involves Functional TLR4 Signaling in Nonparenchymal Cells1 , 2005, The Journal of Immunology.

[29]  Giovanna Angelini,et al.  NK/iDC interaction results in IL-18 secretion by DCs at the synaptic cleft followed by NK cell activation and release of the DC maturation factor HMGB1. , 2005, Blood.

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

[31]  M. Lotze,et al.  Addicted to Death: Invasive Cancer and the Immune Response to Unscheduled Cell Death , 2005, Journal of immunotherapy.

[32]  Masaki Tanaka,et al.  Contributions of high mobility group box protein in experimental and clinical acute lung injury. , 2004, American journal of respiratory and critical care medicine.

[33]  K. Takata,et al.  High mobility group box protein‐1 inhibits microglial Aβ clearance and enhances Aβ neurotoxicity , 2004 .

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

[35]  K. Tracey,et al.  High Mobility Group Box Protein 1: An Endogenous Signal for Dendritic Cell Maturation and Th1 Polarization , 2004, The Journal of Immunology.

[36]  Polly Matzinger,et al.  Hydrophobicity: an ancient damage-associated molecular pattern that initiates innate immune responses , 2004, Nature Reviews Immunology.

[37]  S. Müller,et al.  Regulated expression and subcellular localization of HMGB1, a chromatin protein with a cytokine function , 2004, Journal of internal medicine.

[38]  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.

[39]  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.

[40]  K. Tracey,et al.  Activation of gene expression in human neutrophils by high mobility group box 1 protein. , 2003, American journal of physiology. Cell physiology.

[41]  M. Bianchi,et al.  The nuclear protein HMGB1 is secreted by monocytes via a non‐classical, vesicle‐mediated secretory pathway , 2002, EMBO reports.

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

[43]  W. Fang,et al.  The Significance of Changes in High Mobility Group-1 Protein mRNA Expression in Rats After Thermal Injury , 2002, Shock.

[44]  A. Nakagawara,et al.  HMGB1 and HMGB2 Cell-specifically Down-regulate the p53- and p73-dependent Sequence-specific Transactivation from the Human Bax Gene Promoter* , 2002, The Journal of Biological Chemistry.

[45]  K. Tracey,et al.  Cutting Edge: HMG-1 as a Mediator of Acute Lung Inflammation1 , 2000, The Journal of Immunology.

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

[47]  J. Chen,et al.  The Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin , 1995, The Journal of Biological Chemistry.

[48]  T. Misteli,et al.  Release of chromatin protein HMGB1 by necrotic cells triggers inflammation , 2010, Nature.

[49]  A. Castiglioni,et al.  High-mobility group box 1 (HMGB1) as a master regulator of innate immunity , 2010, Cell and Tissue Research.

[50]  K. Takata,et al.  High mobility group box protein-1 inhibits microglial Abeta clearance and enhances Abeta neurotoxicity. , 2004, Journal of neuroscience research.