Treatment with GITR agonistic antibody corrects adaptive immune dysfunction in sepsis
Open Access
- 15 November 2007
- journal article
- research article
- Published by American Society of Hematology in Blood
- Vol. 110 (10) , 3673-3681
- https://doi.org/10.1182/blood-2007-04-087171
Abstract
Apoptosis of CD4+ T cells and TH2 polarization are hallmarks of sepsis-induced immunoparalysis. In this study, we characterized sepsis-induced adaptiKeywords
This publication has 30 references indexed in Scilit:
- THE CONTRIBUTION OF CD4+ CD25+ T-REGULATORY-CELLS TO IMMUNE SUPPRESSION IN SEPSISShock, 2007
- The Adaptor Molecule MyD88 Activates PI-3 Kinase Signaling in CD4+ T Cells and Enables CpG Oligodeoxynucleotide-Mediated CostimulationImmunity, 2006
- In vivo delivery of caspase-8 or Fas siRNA improves the survival of septic miceBlood, 2005
- GITR: a multifaceted regulator of immunity belonging to the tumor necrosis factor receptor superfamilyEuropean Journal of Immunology, 2005
- TCR ζ-chain downregulation: curtailing an excessive inflammatory immune responseNature Reviews Immunology, 2004
- Arginase I Production in the Tumor Microenvironment by Mature Myeloid Cells Inhibits T-Cell Receptor Expression and Antigen-Specific T-Cell ResponsesCancer Research, 2004
- Frontline: GITR, a member of the TNF receptor superfamily, is costimulatory to mouse T lymphocyte subpopulationsEuropean Journal of Immunology, 2004
- Toll Pathway-Dependent Blockade of CD4 + CD25 + T Cell-Mediated Suppression by Dendritic CellsScience, 2003
- Stimulation of CD25+CD4+ regulatory T cells through GITR breaks immunological self-toleranceNature Immunology, 2002
- Host Resistance in Sepsis and TraumaAnnals of Surgery, 1975