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Critical Reviews™ in Immunology

Impact factor: 3.698

ISSN Print: 1040-8401
ISSN Online: 2162-6472

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2013006721
pages 23-40

T-Cell-Mediated Immunity and the Role of TRAIL in Sepsis-Induced Immunosuppression

Stephanie A. Condotta
Department of Pathology, University of Iowa, Iowa City, Iowa
Javier Cabrera-Perez
Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, Minnesota
Vladimir P. Badovinac
Department of Pathology, Interdisciplinary Program in Immunology, University of Iowa, Iowa City, Iowa
Thomas S. Griffith
Department of Urology, University of Minnesota, Minneapolis, MN; Microbiology, Immunology and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, MN; Center for Immunology, University of Minnesota, Minneapolis, MN; Minneapolis VA Health Care System, Minneapolis, Minnesota

ABSTRACT

Sepsis is the leading cause of death in most intensive care units, and the death of septic patients usually does not result from the initial septic event but rather from subsequent nosocomial infections. Patients who survive severe sepsis often display severely compromised immune function. Not only is there significant apoptosis of lymphoid and myeloid cells that depletes critical components of the immune system during sepsis, there is also decreased function of the remaining immune cells. Studies of animals and humans suggest the immune defects that occur during sepsis may be critical to pathogenesis and subsequent mortality. This review focuses on sepsis-induced alterations with the cluster differentiation (CD) 8 T-cell compartment that can affect the control of secondary heterologous infections. Understanding how a septic event directly influences CD8 T-cell populations through apoptotic death and homeostatic proliferation and indirectly by immune-mediated suppression will provide valuable starting points for developing new treatment options.