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Infection and Immunity, January 2006, p. 282-288, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.282-288.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Differential Regulation of Cytokine Production by CD1d-Restricted NKT Cells in Response to Superantigen Staphylococcal Enterotoxin B Exposure

Melanie J. Ragin,1,2 Nisebita Sahu,1,3 and Avery August1*

Center for Molecular Immunology & Infectious Disease and Department of Veterinary and Biomedical Sciences,1 Pathobiology Graduate Program,2 Department of Biochemistry & Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 168023

Received 20 September 2005/ Returned for modification 8 October 2005/ Accepted 13 October 2005

NKT cells are a heterogeneous population characterized by the ability to rapidly produce cytokines, such as interleukin 2 (IL-2), IL-4, and gamma interferon (IFN-{gamma}) in response to infections by viruses, bacteria, and parasites. The bacterial superantigen staphylococcal enterotoxin B (SEB) interacts with T cells bearing the Vß3, -7, or -8 T-cell receptors, inducing their expansion and cytokine secretion, leading to death in some cases due to cytokine poisoning. The majority of NKT cells bear the Vß7 or -8 T-cell receptor, suggesting that they may play a role in regulating this response. Using mice lacking NKT cells (CD1d–/– and J{alpha}18–/– mice), we set out to identify the role of these cells in T-cell expansion, cytokine secretion, and toxicity induced by exposure to SEB. We find that Vß8+ CD4+ T-cell populations similarly expand in wild-type (WT) and NKT cell-null mice and that NKT cells did not regulate the secretion of IL-2. By contrast, these cells positively regulated the secretion of IL-4 and IFN-{gamma} production and negatively regulated the secretion of tumor necrosis factor alpha (TNF-{alpha}). However, this negative regulation of TNF-{alpha} secretion by NKT cells provides only a minor protective effect on SEB-mediated shock in WT mice compared to mice lacking NKT cells. These data suggest that NKT cells may regulate the nature of the cytokine response to exposure to the superantigen SEB and may act as regulatory T cells during exposure to this superantigen.

* Corresponding author. Mailing address: Center for Molecular Immunology & Infectious Disease, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, 115 Henning Building, University Park, PA 16803. Phone: (814) 863-3539. Fax: (814) 863-6140. E-mail: avery{at}psu.edu.

Editor: J. T. Barbieri

Infection and Immunity, January 2006, p. 282-288, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.282-288.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.





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