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The gamma interferon (IFN-\u03b3) response is deeply affected in both extremes. The implication of IFN-\u03b3 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-\u03b3 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-\u03b3 serum release 72 h after priming. However, at this time, a selective blockade of IFN-\u03b3\/STAT1 signaling develops in spleen cells, correlating with a lack of expression of the IFN-\u03b3 receptor beta subunit and STAT1 in the T-cell population. Selective blockade of the STAT1 signaling pathway\u2014while simultaneously maintaining STAT3 signaling and expression\u2014may be a protective mechanism that shortens IFN-\u03b3 production during the Th1 effector response. This blockade may also have consequences on switching towards a suppressor phenotype with chronic exposure to the superantigen.<\/jats:p>","DOI":"10.1128\/iai.01220-06","type":"journal-article","created":{"date-parts":[[2006,12,20]],"date-time":"2006-12-20T23:51:25Z","timestamp":1166658685000},"page":"306-313","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["Staphylococcal Enterotoxin B In Vivo Modulates both Gamma Interferon Receptor Expression and Ligand-Induced Activation of Signal Transducer and Activator of Transcription 1 in T Cells"],"prefix":"10.1128","volume":"75","author":[{"given":"R.","family":"Plaza","sequence":"first","affiliation":[{"name":"Department of Immunology, Hospital de la Santa Creu i Sant Pau, Universitat Auto\u0300noma de Barcelona, Avda. Sant Antoni Maria Claret 167, Barcelona 08025, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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