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This article has been retracted as it is essentially identical in content with the published article “NKT Cells: The Culprits of Sepsis?,” Briana Leung and Hobart W. Harris, Journal of Surgical Research, Volume 167, Issue 1, Pages 87-95, 1 May 2011.

Clinical and Developmental Immunology
Volume 2010 (2010), Article ID 414650, 10 pages
Review Article

NKT Cells in Sepsis

Department of Surgery, University of California, San Francisco, San Francisco, CA 94143, USA

Received 29 June 2010; Revised 30 August 2010; Accepted 30 August 2010

Academic Editor: Toshinori Nakayama

Copyright © 2010 Briana Leung and Hobart W. Harris. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sepsis is currently a leading cause of death in hospital intensive care units. Previous studies suggest that the pathophysiology of sepsis involves the hyperactivation of complex proinflammatory cascades that include the activation of various immune cells and the exuberant secretion of proinflammatory cytokines by these cells. Natural killer T-cells (NKTs) are a sublineage of T cells that share characteristics of conventional T cells and NK cells and bridge innate and adaptive immunity. More recently, NKT cells have been implicated in microbial immunity, including the onset of sepsis. Moreover, apolipoprotein E (apoE), a component of triglyceride-rich lipoproteins, has been shown to be protective in endotoxemia and gram-negative infections in addition to its well-known role in lipid metabolism. Here, we will review the role of NKT cells in sepsis and septic shock, the immunoregulatory role of apoE in the host immune response to infection, and propose a mechanism for this immunoregulation.