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Infection and Immunity, January 2007, p. 306-313, Vol. 75, No. 1
0019-9567/07/$08.00+0 doi:10.1128/IAI.01220-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Immunology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Avda. Sant Antoni Maria Claret 167, Barcelona 08025, Spain
Received 2 August 2006/ Returned for modification 15 September 2006/ Accepted 19 October 2006
Superantigens (SAg) are bacterial exotoxins that provoke extreme responses in the immune system; for example, the acute hyperactivation of SAg-reactive T cells that leads to toxic shock syndrome is followed within days by strong immunosuppression. The gamma interferon (IFN-
) response is deeply affected in both extremes. The implication of IFN-
in the pathophysiology of lethal shock induced in mice after a secondary challenge with the SAg staphylococcal enterotoxin B (SEB) prompted us to study the regulation of IFN-
secretion and the intracellular response. We demonstrate in this study that a rechallenge with SEB becomes lethal only when given inside a critical time window after SEB priming and is associated with an increase of IFN-
serum release 72 h after priming. However, at this time, a selective blockade of IFN-
/STAT1 signaling develops in spleen cells, correlating with a lack of expression of the IFN-
receptor beta subunit and STAT1 in the T-cell population. Selective blockade of the STAT1 signaling pathwaywhile simultaneously maintaining STAT3 signaling and expressionmay be a protective mechanism that shortens IFN-
production during the Th1 effector response. This blockade may also have consequences on switching towards a suppressor phenotype with chronic exposure to the superantigen.
Published ahead of print on 30 October 2006.
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