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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Immunology
Импакт фактор: 1.352 5-летний Импакт фактор: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Печать: 1040-8401
ISSN Онлайн: 2162-6472

Выпуски:
Том 39, 2019 Том 38, 2018 Том 37, 2017 Том 36, 2016 Том 35, 2015 Том 34, 2014 Том 33, 2013 Том 32, 2012 Том 31, 2011 Том 30, 2010 Том 29, 2009 Том 28, 2008 Том 27, 2007 Том 26, 2006 Том 25, 2005 Том 24, 2004 Том 23, 2003 Том 22, 2002 Том 21, 2001 Том 20, 2000 Том 19, 1999 Том 18, 1998 Том 17, 1997 Том 16, 1996 Том 15, 1995 Том 14, 1994

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

Краткое описание

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.


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