Abstract |
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-gamma) response is deeply affected in both extremes. The implication of IFN-gamma 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-gamma 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-gamma serum release 72 h after priming. However, at this time, a selective blockade of IFN-gamma/STAT1 signaling develops in spleen cells, correlating with a lack of expression of the IFN-gamma receptor beta subunit and STAT1 in the T-cell population. Selective blockade of the STAT1 signaling pathway--while simultaneously maintaining STAT3 signaling and expression--may be a protective mechanism that shortens IFN-gamma production during the Th1 effector response. This blockade may also have consequences on switching towards a suppressor phenotype with chronic exposure to the superantigen.
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Authors | R Plaza, J L Rodriguez-Sanchez, C Juarez |
Journal | Infection and immunity
(Infect Immun)
Vol. 75
Issue 1
Pg. 306-13
(Jan 2007)
ISSN: 0019-9567 [Print] United States |
PMID | 17074848
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antigens, Bacterial
- Enterotoxins
- Ligands
- Receptors, Interferon
- STAT1 Transcription Factor
- Stat1 protein, mouse
- Superantigens
- interferon gamma receptor
- enterotoxin B, staphylococcal
- Interferon-gamma
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Topics |
- Animals
- Antigens, Bacterial
(immunology)
- Electrophoretic Mobility Shift Assay
- Enterotoxins
(immunology)
- Escherichia coli
(immunology)
- Immune Tolerance
- Interferon-gamma
(biosynthesis)
- Ligands
- Lymphocyte Activation
(immunology)
- Mice
- Mice, Inbred BALB C
- Receptors, Interferon
(biosynthesis)
- Reverse Transcriptase Polymerase Chain Reaction
- STAT1 Transcription Factor
(immunology, metabolism)
- Shock, Septic
(immunology)
- Signal Transduction
(immunology)
- Superantigens
(immunology)
- Th1 Cells
(immunology)
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