Research Topics
Species | James A LedererSummaryAffiliation: Harvard University Country: USA Publications
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Publications
Burn injury initiates a shift in superantigen-induced T cell responses and host survivalYan 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...
Regulatory T cells suppress antigen-driven CD4 T cell reactivity following injuryMalcolm 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...- Comparison of longitudinal leukocyte gene expression after burn injury or trauma-hemorrhage in miceJames A Lederer
Department of Surgery, Brigham and Women s Hospital Harvard Medical School, Boston, Massachusetts 02115, USA
Physiol Genomics 32:299-310. 2008.... - Murine dendritic cell antigen-presenting cell function is not altered by burn injurySatoshi 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... - CD4+CD25+ regulatory T cells control innate immune reactivity after injuryThomas 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... - Linking the "two-hit" response following injury to enhanced TLR4 reactivityThomas 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... - Enhanced regulatory T cell activity is an element of the host response to injuryNiamh 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... - Platelet depletion in mice increases mortality after thermal injurySatoshi 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... - Injury-induced GR-1+ macrophage expansion and activation occurs independently of CD4 T-cell influenceFionnuala 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... - Burn injury induces an early activation response by lymph node CD4+ T cellsElizabeth 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.... - Injury enhances resistance to Escherichia coli infection by boosting innate immune system functionAdrian 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.... - Increased CD4+ CD25+ T regulatory cell activity in trauma patients depresses protective Th1 immunityMalcolm 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..Most significantly, Tregs are important mediators of the suppression of T cell activation and the reduction in TH1 cytokine production found after injury... - Enhanced TLR4 reactivity following injury is mediated by increased p38 activationAdrian 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... - Burn injury promotes antigen-driven Th2-type responses in vivoZhijun 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... - Injury primes the innate immune system for enhanced Toll-like receptor reactivityHugh M Paterson
Department of Surgery, Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115, USA
J Immunol 171:1473-83. 2003.... - Interaction between the innate and adaptive immune systems is required to survive sepsis and control inflammation after injuryOdhran 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... - Injury, sepsis, and the regulation of Toll-like receptor responsesThomas J Murphy
Department of Surgery, Brigham and Women's Hospital, Boston, MA 02115, USA
J Leukoc Biol 75:400-7. 2004.... 
Phospho-flow cytometry based analysis of differences in T cell receptor signaling between regulatory T cells and CD4+ T cellsMarc 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....- A protective role for inflammasome activation following injuryAkinori Osuka
Department of Surgery Immunology, Brigham and Women s Hospital Harvard Medical School, Boston, Massachusetts 02115, USA
Shock 37:47-55. 2012.... - Use of intracellular cytokine staining and bacterial superantigen to document suppression of the adaptive immune system in injured patientsThomas 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..Both T cell subsets show progressive loss of immunostimulatory cytokine production with maintenance of potentially suppressive IL-10 production. These events may have negative consequences for host defense... - Trauma equals danger--damage control by the immune systemVeit 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... - Mast cells and resistance to peritoneal sepsis after burn injuryOdhran 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.... - Microfluidic leukocyte isolation for gene expression analysis in critically ill hospitalized patientsAman 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... - Injury induces early activation of T-cell receptor signaling pathways in CD4+ regulatory T cellsMarc 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... - Differentiation of stress, metabolism, communication, and defense responses following transplantationThomas 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... - B cellsMalcolm MacConmara
Department of Surgery, Brigham and Women's Hospital/Harvard Medical School, Boston, MA, USA
Crit Care Med 33:S514-6. 2005 - Commonality and differences in leukocyte gene expression patterns among three models of inflammation and injuryBernard 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... - Trauma-hemorrhage inhibits splenic dendritic cell proinflammatory cytokine production via a mitogen-activated protein kinase processTakashi 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... - Trauma-hemorrhage induces depressed splenic dendritic cell functions in miceTakashi 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... - Does nitric oxide control the counter-inflammatory response in endotoxic shock?James A Lederer
Crit Care Med 33:896-8. 2005
Research Grants
- INJURY-INDUCED EFFECTS ON THE ADAPTIVE IMMUNE SYSTEMJames 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. ..
- IMMUNOLOGIC STUDIES OF PATIENTS AFTER TRAUMATIC INJURYJames Lederer; Fiscal Year: 2007....
- INJURY INDUCED EFFECTS ON THE ADAPTIVE IMMUNE SYSTEMJames 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. ..
- IMMUNOLOGIC STUDIES OF PATIENTS AFTER TRAUMATIC INJURYJames A Lederer; Fiscal Year: 2010..abstract_text> ..