Anti-HMGB1 Monoclonal Antibody Ameliorates Immunosuppression after Peripheral Tissue Trauma: Attenuated T-Lymphocyte Response and Increased Splenic CD11b+Gr-1+ Myeloid-Derived Suppressor Cells Require HMGB1
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T. Billiar | M. Scott | H. Pape | X. Ruan | Changchun Cai | S. Darwiche
[1] H. Baker,et al. Persistent inflammation, immunosuppression, and catabolism syndrome after severe blunt trauma , 2014, The journal of trauma and acute care surgery.
[2] Y. Vodovotz,et al. The Central Role of Arginine Catabolism in T-Cell Dysfunction and Increased Susceptibility to Infection After Physical Injury , 2014, Annals of surgery.
[3] K. Tao,et al. HMGB1 recruits myeloid derived suppressor cells to promote peritoneal dissemination of colon cancer after resection. , 2013, Biochemical and biophysical research communications.
[4] K. Tracey,et al. The many faces of HMGB1: molecular structure‐functional activity in inflammation, apoptosis, and chemotaxis , 2013, Journal of leukocyte biology.
[5] T. Billiar,et al. Selective roles for toll-like receptors 2, 4, and 9 in systemic inflammation and immune dysfunction following peripheral tissue injury , 2013, The journal of trauma and acute care surgery.
[6] H. Baker,et al. Identification and Description of a Novel Murine Model for Polytrauma and Shock , 2013, Critical care medicine.
[7] S. Singhal,et al. Myeloid derived suppressor cells , 2013, Oncoimmunology.
[8] T. Billiar,et al. Inducible Nitric Oxide Synthase Contributes to Immune Dysfunction Following Trauma , 2012, Shock.
[9] J. Lederer,et al. Trauma equals danger—damage control by the immune system , 2012, Journal of leukocyte biology.
[10] G. Hong,et al. Up-regulation of mitofusin-2 protects CD4+ T cells from HMGB1-mediated immune dysfunction partly through Ca(2+)-NFAT signaling pathway. , 2012, Cytokine.
[11] Kevin W Eliceiri,et al. NIH Image to ImageJ: 25 years of image analysis , 2012, Nature Methods.
[12] John D. Storey,et al. A genomic storm in critically injured humans , 2011, The Journal of experimental medicine.
[13] M. Tsan. Heat shock proteins and high mobility group box 1 protein lack cytokine function , 2011, Journal of leukocyte biology.
[14] T. Billiar,et al. Pseudofracture: an acute peripheral tissue trauma model. , 2011, Journal of visualized experiments : JoVE.
[15] Y. Vodovotz,et al. Models of lower extremity damage in mice: time course of organ damage and immune response. , 2011, The Journal of surgical research.
[16] K. Tracey,et al. HMGB1 is a therapeutic target for sterile inflammation and infection. , 2011, Annual review of immunology.
[17] L. Su,et al. Interleukin-6 Induces Gr-1+CD11b+ Myeloid Cells to Suppress CD8+ T Cell-Mediated Liver Injury in Mice , 2011, PloS one.
[18] Lyle L. Moldawer,et al. A Paradoxical Role for Myeloid-Derived Suppressor Cells in Sepsis and Trauma , 2011, Molecular medicine.
[19] T. Billiar,et al. Role of hemorrhage in the induction of systemic inflammation and remote organ damage: Analysis of combined pseudo‐fracture and hemorrhagic shock , 2011, Journal of orthopaedic research : official publication of the Orthopaedic Research Society.
[20] A. Epstein,et al. Characterization of Cytokine-Induced Myeloid-Derived Suppressor Cells from Normal Human Peripheral Blood Mononuclear Cells , 2010, The Journal of Immunology.
[21] J. Magarian Blander,et al. Hepatic acute-phase proteins control innate immune responses during infection by promoting myeloid-derived suppressor cell function , 2010, The Journal of experimental medicine.
[22] J. Solomkin,et al. Divergent adaptive and innate immunological responses are observed in humans following blunt trauma , 2010, BMC Immunology.
[23] J. Ochoa,et al. Stat 6-Dependent Induction of Myeloid Derived Suppressor Cells After Physical Injury Regulates Nitric Oxide Response to Endotoxin , 2010, Annals of surgery.
[24] Yanghua Qin,et al. HMGB1 Enhances the Proinflammatory Activity of Lipopolysaccharide by Promoting the Phosphorylation of MAPK p38 through Receptor for Advanced Glycation End Products1 , 2009, The Journal of Immunology.
[25] E. Abraham. Unraveling the role of high mobility group box protein 1 in severe trauma , 2009, Critical care.
[26] I. Chaudry,et al. Suppression of activation and costimulatory signaling in splenic CD4+ T cells after trauma-hemorrhage reduces T-cell function: a mechanism of post-traumatic immune suppression. , 2009, The American journal of pathology.
[27] U. Andersson,et al. The alarmin HMGB1 acts in synergy with endogenous and exogenous danger signals to promote inflammation , 2009, Journal of leukocyte biology.
[28] A. Sauaia,et al. HMGB1 IS MARKEDLY ELEVATED WITHIN 6 HOURS OF MECHANICAL TRAUMA IN HUMANS , 2009, Shock.
[29] Srinivas Nagaraj,et al. Myeloid-derived suppressor cells as regulators of the immune system , 2009, Nature Reviews Immunology.
[30] F. Schade,et al. Invited review: Deterioration of the immune system after trauma: signals and cellular mechanisms , 2008, Innate immunity.
[31] D. Foell,et al. Proinflammatory S100 Proteins Regulate the Accumulation of Myeloid-Derived Suppressor Cells1 , 2008, The Journal of Immunology.
[32] I. Chaudry,et al. Estrogen: A Novel Therapeutic Adjunct for the Treatment of Trauma-Hemorrhage—Induced Immunological Alterations , 2008, Molecular medicine.
[33] E. Abraham,et al. HMGB1 Develops Enhanced Proinflammatory Activity by Binding to Cytokines1 , 2008, The Journal of Immunology.
[34] J. Leips,et al. Reduced inflammation in the tumor microenvironment delays the accumulation of myeloid-derived suppressor cells and limits tumor progression. , 2007, Cancer research.
[35] L. Moldawer,et al. MyD88-dependent expansion of an immature GR-1+CD11b+ population induces T cell suppression and Th2 polarization in sepsis , 2007, The Journal of experimental medicine.
[36] L. Audoly,et al. Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE , 2007, Nature Immunology.
[37] D. Angus,et al. Circulating high-mobility group box 1 (HMGB1) concentrations are elevated in both uncomplicated pneumonia and pneumonia with severe sepsis* , 2007, Critical care medicine.
[38] H. Rauvala,et al. Analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin) , 2007, Journal of leukocyte biology.
[39] M. Bianchi. Interview with Dr. Heikki Rauvala regarding Pivotal Advance: Analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin) , 2007, Journal of leukocyte biology.
[40] I. Chaudry,et al. Lidocaine depresses splenocyte immune functions following trauma-hemorrhage in mice. , 2006, American journal of physiology. Cell physiology.
[41] O. Levy,et al. TCR ζ Down-Regulation under Chronic Inflammation Is Mediated by Myeloid Suppressor Cells Differentially Distributed between Various Lymphatic Organs1 , 2006, The Journal of Immunology.
[42] K. Tracey,et al. Anti-HMGB1 Neutralizing Antibody Ameliorates Gut Barrier Dysfunction and Improves Survival after Hemorrhagic Shock , 2006, Molecular medicine.
[43] J. Ochoa,et al. CD11b+/Gr-1+ Myeloid Suppressor Cells Cause T Cell Dysfunction after Traumatic Stress1 , 2006, The Journal of Immunology.
[44] M. Keel,et al. Pathophysiology of polytrauma. , 2005, Injury.
[45] I. Chaudry,et al. Transgenic prolactin-/- mice: effect of trauma-hemorrhage on splenocyte functions. , 2005, American journal of physiology. Cell physiology.
[46] K. Tracey,et al. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion , 2005, The Journal of experimental medicine.
[47] B. Fingleton,et al. Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis. , 2004, Cancer cell.
[48] Haichao Wang,et al. Bench to bedside: HMGB1-a novel proinflammatory cytokine and potential therapeutic target for septic patients in the emergency department. , 2004, Academic emergency medicine : official journal of the Society for Academic Emergency Medicine.
[49] J. Puyana,et al. Both T-helper-1- and T-helper-2-type lymphokines are depressed in posttrauma anergy. , 1998, The Journal of trauma.
[50] F. Schildberg,et al. Postburn constitutional changes in T-cell reactivity occur in CD8+ rather than in CD4+ cells. , 1997, The Journal of trauma.
[51] A. Kelso. Th1 and Th2 subsets: paradigms lost? , 1995, Immunology today.
[52] J. Mannick,et al. Altered Gene Transcription After Burn Injury Results in Depressed T‐Lymphocyte Activation , 1994, Annals of surgery.
[53] J. L. Rodriguez,et al. Lymphocyte subset responses to trauma and sepsis. , 1993, The Journal of trauma.
[54] S. Jonjić,et al. Site-restricted persistent cytomegalovirus infection after selective long-term depletion of CD4+ T lymphocytes , 1989, The Journal of experimental medicine.
[55] A. Munster. POST-TRAUMATIC IMMUNOSUPPRESSION IS DUE TO ACTIVATION OF SUPPRESSOR T CELLS , 1976, The Lancet.
[56] Anne S Frankel,et al. National Institutes of Health , 2019, The Grants Register 2022.
[57] C. Divino,et al. Immune stimulatory receptor CD40 is required for T-cell suppression and T regulatory cell activation mediated by myeloid-derived suppressor cells in cancer. , 2010, Cancer research.
[58] L. Audoly,et al. Toll-like receptor 9 – dependent activation by DNA-containing immune complexes is mediated by HMGB 1 and RAGE , 2007 .
[59] A. Sauaia,et al. Epidemiology of trauma deaths: a reassessment. , 1993, The Journal of trauma.
[60] J. Lenihan,et al. Staff-location systems suitable for hospital use. , 1958, Lancet.