James A Lederer

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Burn injury initiates a shift in superantigen-induced T cell responses and host survival
    Yan Zang
    Department of Surgery, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 172:4883-92. 2004
  2. pmc Regulatory T cells suppress antigen-driven CD4 T cell reactivity following injury
    Malcolm P MacConmara
    Department of Surgery, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Leukoc Biol 89:137-47. 2011
  3. ncbi request reprint Comparison of longitudinal leukocyte gene expression after burn injury or trauma-hemorrhage in mice
    James A Lederer
    Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, Massachusetts 02115, USA
    Physiol Genomics 32:299-310. 2008
  4. ncbi request reprint CD4+CD25+ regulatory T cells control innate immune reactivity after injury
    Thomas J Murphy
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 174:2957-63. 2005
  5. ncbi request reprint Linking the "two-hit" response following injury to enhanced TLR4 reactivity
    Thomas J Murphy
    Department of Surgery Immunology, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    J Leukoc Biol 77:16-23. 2005
  6. pmc Murine dendritic cell antigen-presenting cell function is not altered by burn injury
    Satoshi Fujimi
    Department of Surgery, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    J Leukoc Biol 85:862-70. 2009
  7. ncbi request reprint Enhanced regulatory T cell activity is an element of the host response to injury
    Niamh Ni Choileain
    Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    J Immunol 176:225-36. 2006
  8. pmc Platelet depletion in mice increases mortality after thermal injury
    Satoshi Fujimi
    Julian and Eunice Cohen Laboratory for Surgical Research, Department of Surgery, Brigham and Women s Hospital, Boston, MA 02115, USA
    Blood 107:4399-406. 2006
  9. pmc Injury-induced GR-1+ macrophage expansion and activation occurs independently of CD4 T-cell influence
    Fionnuala M O'Leary
    Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    Shock 36:162-9. 2011
  10. ncbi request reprint Injury enhances resistance to Escherichia coli infection by boosting innate immune system function
    Adrian A Maung
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    J Immunol 180:2450-8. 2008

Research Grants

Collaborators

Detail Information

Publications32

  1. ncbi request reprint Burn injury initiates a shift in superantigen-induced T cell responses and host survival
    Yan Zang
    Department of Surgery, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 172:4883-92. 2004
    ..Although prior studies link this counterinflammatory-type response to lowered resistance to infection, the present results suggest it may sometimes benefit the injured host...
  2. pmc Regulatory T cells suppress antigen-driven CD4 T cell reactivity following injury
    Malcolm P MacConmara
    Department of Surgery, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Leukoc Biol 89:137-47. 2011
    ..Taken together, these findings demonstrate that Tregs can actively control the in vivo expansion and reactivity of antigen-stimulated, naïve CD4 T cells following severe injury...
  3. ncbi request reprint Comparison of longitudinal leukocyte gene expression after burn injury or trauma-hemorrhage in mice
    James A Lederer
    Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, Massachusetts 02115, USA
    Physiol Genomics 32:299-310. 2008
    ....
  4. ncbi request reprint CD4+CD25+ regulatory T cells control innate immune reactivity after injury
    Thomas J Murphy
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 174:2957-63. 2005
    ..These findings suggest a previously unsuspected role for CD4(+)CD25(+) T regulatory cells in controlling host inflammatory responses after injury...
  5. ncbi request reprint Linking the "two-hit" response following injury to enhanced TLR4 reactivity
    Thomas J Murphy
    Department of Surgery Immunology, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    J Leukoc Biol 77:16-23. 2005
    ..These findings demonstrate the potential lethality of excessive TLR4 reactivity after injury and provide an explanation for the exaggerated inflammatory response to a second hit, which can occur following severe injury...
  6. pmc Murine dendritic cell antigen-presenting cell function is not altered by burn injury
    Satoshi Fujimi
    Department of Surgery, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    J Leukoc Biol 85:862-70. 2009
    ..Taken together, these findings support the conclusion that DC do not acquire a suppressive phenotype following severe injury in mice...
  7. ncbi request reprint Enhanced regulatory T cell activity is an element of the host response to injury
    Niamh Ni Choileain
    Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    J Immunol 176:225-36. 2006
    ..Taken together, these observations suggest that injury can induce or amplify CD4+CD25+ Treg function and that CD4+CD25+ T cells contribute to the development of postinjury immune suppression...
  8. pmc Platelet depletion in mice increases mortality after thermal injury
    Satoshi Fujimi
    Julian and Eunice Cohen Laboratory for Surgical Research, Department of Surgery, Brigham and Women s Hospital, Boston, MA 02115, USA
    Blood 107:4399-406. 2006
    ..Moreover, our findings suggest that platelets and, more importantly, platelet-derived TGFbeta(1) modulate the systemic inflammatory response occurring after injury...
  9. pmc Injury-induced GR-1+ macrophage expansion and activation occurs independently of CD4 T-cell influence
    Fionnuala M O'Leary
    Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    Shock 36:162-9. 2011
    ..These data suggest that modulating GR-1 macrophage activation as well as CD4 T cell responses after severe injury may help control the development of systemic inflammatory response syndrome and the two-hit response phenotype...
  10. ncbi request reprint Injury enhances resistance to Escherichia coli infection by boosting innate immune system function
    Adrian A Maung
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    J Immunol 180:2450-8. 2008
    ....
  11. pmc Increased CD4+ CD25+ T regulatory cell activity in trauma patients depresses protective Th1 immunity
    Malcolm P MacConmara
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Ann Surg 244:514-23. 2006
    ..This study sought to determine if Tregs mediate the reduction in TH1-type immunity after serious injury in man and if Treg function is altered by injury...
  12. ncbi request reprint Burn injury induces an early activation response by lymph node CD4+ T cells
    Elizabeth M Purcell
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    Shock 25:135-40. 2006
    ....
  13. ncbi request reprint Enhanced TLR4 reactivity following injury is mediated by increased p38 activation
    Adrian A Maung
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Leukoc Biol 78:565-73. 2005
    ..Our results suggest that the injury-induced increase in TLR4 reactivity is mediated, at least in part, by enhanced activation of the p38 signaling pathway...
  14. ncbi request reprint Burn injury promotes antigen-driven Th2-type responses in vivo
    Zhijun Guo
    Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    J Immunol 171:3983-90. 2003
    ..These findings establish that severe injury induces fundamental changes in the induction of Ag-specific CD4(+) Th cell responses favoring the development of Th2-type immune reactivity in vivo...
  15. ncbi request reprint Injury primes the innate immune system for enhanced Toll-like receptor reactivity
    Hugh M Paterson
    Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    J Immunol 171:1473-83. 2003
    ....
  16. ncbi request reprint Injury, sepsis, and the regulation of Toll-like receptor responses
    Thomas J Murphy
    Department of Surgery, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Leukoc Biol 75:400-7. 2004
    ....
  17. ncbi request reprint Interaction between the innate and adaptive immune systems is required to survive sepsis and control inflammation after injury
    Odhran Shelley
    Department of Surgery, Harvard Medical School, Boston, MA 02115, USA
    Shock 20:123-9. 2003
    ..These studies demonstrate that the adaptive immune system is necessary for protection from polymicrobial sepsis and plays a significant role in regulating the inflammatory response to injury...
  18. doi request reprint Phospho-flow cytometry based analysis of differences in T cell receptor signaling between regulatory T cells and CD4+ T cells
    Marc Hanschen
    Department of Surgery Immunology, Brigham and Women s Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, United States
    J Immunol Methods 376:1-12. 2012
    ....
  19. pmc A protective role for inflammasome activation following injury
    Akinori Osuka
    Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, Massachusetts 02115, USA
    Shock 37:47-55. 2012
    ....
  20. pmc Use of intracellular cytokine staining and bacterial superantigen to document suppression of the adaptive immune system in injured patients
    Thomas Murphy
    Department of Surgery, Julian and Eunice Cohen Laboratory, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Ann Surg 238:401-10; discussion 410-1. 2003
    ....
  21. pmc Mesenchymal stromal cells improve survival during sepsis in the absence of heme oxygenase-1: the importance of neutrophils
    Sean R R Hall
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women s Hospital Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts, USA
    Stem Cells 31:397-407. 2013
    ....
  22. pmc Chronic endotoxin exposure produces airflow obstruction and lung dendritic cell expansion
    Peggy S Lai
    Harvard School of Public Health, Boston, Massachusetts, USA
    Am J Respir Cell Mol Biol 47:209-17. 2012
    ..These findings point to a novel underlying mechanism of airflow obstruction as a result of occupational LPS exposure, and suggest molecular and cellular targets for therapeutic development...
  23. pmc Trauma equals danger--damage control by the immune system
    Veit M Stoecklein
    Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, MA, USA
    J Leukoc Biol 92:539-51. 2012
    ..Additionally, we review and propose strategies for redirecting injury responses to help restore immune system homeostasis...
  24. doi request reprint Microfluidic leukocyte isolation for gene expression analysis in critically ill hospitalized patients
    Aman Russom
    Surgical Services and Center for Engineering in Medicine, Massachusetts General Hospital, Harvard Medical School and Shriners Hospital for Children, Boston, MA, USA
    Clin Chem 54:891-900. 2008
    ..Here, we report the clinical validation of a novel microfluidic leukocyte nucleic acid isolation technique for gene expression analysis from critically ill, hospitalized patients that can be readily used on small volumes of blood...
  25. ncbi request reprint Mast cells and resistance to peritoneal sepsis after burn injury
    Odhran Shelley
    Department of Surgery, Julian and Eunice Cohen Laboratory, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Shock 19:513-8. 2003
    ....
  26. pmc Injury induces early activation of T-cell receptor signaling pathways in CD4+ regulatory T cells
    Marc Hanschen
    Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, MA 02115, USA
    Shock 35:252-7. 2011
    ..These findings suggest that injury provides an early TCR-activating signal to Tregs and supply new insights into how injury influences the adaptive immune system...
  27. ncbi request reprint Differentiation of stress, metabolism, communication, and defense responses following transplantation
    Thomas F Mueller
    Laboratory of Molecular Immunology, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Leukoc Biol 73:379-90. 2003
    ..Innate and adaptive immune responses induced a transcriptional shift toward defense and cell communication. The kinetic analysis showed a shift from innate toward adaptive responses in the post-transplant course...
  28. ncbi request reprint B cells
    Malcolm MacConmara
    Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, MA, USA
    Crit Care Med 33:S514-6. 2005
  29. ncbi request reprint Commonality and differences in leukocyte gene expression patterns among three models of inflammation and injury
    Bernard H Brownstein
    Department of Genetics, Washington University, St Louis, Missouri, USA
    Physiol Genomics 24:298-309. 2006
    ..Although there is some commonality among the models, the majority of the differentially expressed genes appear to be uniquely associated with the type of injury and/or the inflammatory stimulus...
  30. ncbi request reprint Does nitric oxide control the counter-inflammatory response in endotoxic shock?
    James A Lederer
    Crit Care Med 33:896-8. 2005
  31. ncbi request reprint Trauma-hemorrhage induces depressed splenic dendritic cell functions in mice
    Takashi Kawasaki
    Center for Surgical Research and Department of Surgery, University of Alabama, 1670 University Boulevard, Birmingham, AL 35294, USA
    J Immunol 177:4514-20. 2006
    ..This depression in Ag presentation could contribute to the host's enhanced susceptibility to sepsis following T-H...
  32. doi request reprint Trauma-hemorrhage inhibits splenic dendritic cell proinflammatory cytokine production via a mitogen-activated protein kinase process
    Takashi Kawasaki
    Center for Surgical Research, Univ of Alabama at Birmingham, 1670 Univ Blvd, Volker Hall, Rm G094, Birmingham, AL 35294 0019, USA
    Am J Physiol Cell Physiol 294:C754-64. 2008
    ..Hyporesponsiveness of splenic DCs was also found after stimulation with the TLR2 agonist zymosan. Our results may thus explain the profound immunosuppression that is known to occur under those conditions...

Research Grants15

  1. INJURY-INDUCED EFFECTS ON THE ADAPTIVE IMMUNE SYSTEM
    James Lederer; Fiscal Year: 2007
    ..It is hoped that the results of these studies will advance the development of treatments designed to prevent the development of immune system failure and infectious complications following severe injury. ..
  2. IMMUNOLOGIC STUDIES OF PATIENTS AFTER TRAUMATIC INJURY
    James Lederer; Fiscal Year: 2007
    ....
  3. INJURY INDUCED EFFECTS ON THE ADAPTIVE IMMUNE SYSTEM
    James Lederer; Fiscal Year: 2003
    ..The results may also contribute new information leading to the development of novel therapeutic approaches for preventing injury-induced immune dysfunction. ..
  4. IMMUNOLOGIC STUDIES OF PATIENTS AFTER TRAUMATIC INJURY
    James A Lederer; Fiscal Year: 2010
    ..abstract_text> ..