Staphylococcal enterotoxin B induces anergy to conventional peptide in memory T cells

2003 ◽  
Vol 222 (2) ◽  
pp. 144-155 ◽  
Author(s):  
Andrew R.O. Watson ◽  
James N. Mittler ◽  
William T. Lee
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B

scholarly journals Memory T cells are anergic to the superantigen staphylococcal enterotoxin B.

1992 ◽  
Vol 176 (2) ◽  
pp. 575-579 ◽  
Author(s):  
W T Lee ◽  
E S Vitetta
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Staphylococcal Enterotoxin ◽  
Peripheral Tolerance ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B

We have used staphylococcal enterotoxin B (SEB) to study the role of naive and memory T cells in the induction of peripheral tolerance. After administration of SEB to mice, the numbers of naive and memory T cells increase, as does the proportion of memory T cells, which are unresponsive to further stimulation with SEB in vitro. In addition, memory T cells generated in response to conventional antigen, which proliferate and provide help to B cells in the presence of the conventional antigen, fail to respond to superantigen. Hence, memory T cells, in general, are anergized by SEB. These results suggest that SEB-induced activation and anergy reflect the combined responses of naive and memory T cells. The differential activation vs. anergy of naive and memory T cells by superantigen may be related to cytokine production and may play an important role in the etiology of autoimmune diseases or immunodeficiency diseases such as acquired immune deficiency syndrome.

Application of staphylococcal enterotoxin B on normal and atopic skin induces up-regulation of T cells by a superantigen-mediated mechanism

2000 ◽  
Vol 105 (4) ◽  
pp. 820-826 ◽  
Author(s):  
Lone Skov ◽  
Jeanett V. Olsen ◽  
Ralph Giorno ◽  
Patrick M. Schlievert ◽  
Ole Baadsgaard ◽  
...  
Keyword(s):  
T Cells ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Atopic Skin ◽  
Enterotoxin B

Human Eosinophils Enhance Staphylococcal Enterotoxin B Stimulation of CD4+ T-cells

2006 ◽  
Vol 117 (2) ◽  
pp. S62
Author(s):  
S.K. Mathur ◽  
E.A. Durocher ◽  
L. Liu ◽  
E.A.B. Kelly ◽  
J.B. Sedgwick ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B ◽  
Stimulation Of

scholarly journals Induction of unresponsiveness and impaired T cell expansion by staphylococcal enterotoxin B in CD28-deficient mice.

1996 ◽  
Vol 183 (6) ◽  
pp. 2481-2488 ◽  
Author(s):  
H W Mittrücker ◽  
A Shahinian ◽  
D Bouchard ◽  
T M Kündig ◽  
T W Mak
Keyword(s):  
T Cells ◽  
T Cell ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Rapid Induction ◽  
Cd28 Costimulation ◽  
Enterotoxin B ◽  
Deficient Mice

We used CD28-deficient mice to analyze the importance of CD28 costimulation for the response against Staphylococcal enterotoxin B (SEB) in vivo. CD28 was necessary for the strong expansion of V beta 8+ T cells, but not for deletion. The lack of expansion was not due to a failure of SEB to activate V beta 8+ T cells, as V beta 8+ T cells from both CD28-/- and CD28+/+ mice showed similar phenotypic changes within the first 24 h after SEB injection and cell cycle analysis showed that an equal percentage of V beta 8+ T cells started to proliferate. However, the phenotype and the state of proliferation of V beta 8+ T cells was different at later time points. Furthermore, in CD28-/- mice injection with SEB led to rapid induction of unresponsiveness in SEB responsive T cells, indicated by a drastic reduction of proliferation after secondary SEB stimulation in vitro. Unresponsiveness could also be demonstrated in vivo, as CD28-/- mice produced only marginal amounts of TNF alpha after rechallenge with SEB. In addition CD28-/- mice were protected against a lethal toxic shock induced by a second injection with SEB. Our results indicate that CD28 costimulation is crucial for the T cell-mediated toxicity of SEB and demonstrate that T cell stimulation in the absence of CD28 costimulation induces unresponsiveness in vivo.

Orally administered cholera toxin prevents murine intestinal T cells from staphylococcal enterotoxin B-induced anergy

1998 ◽  
Vol 115 (5) ◽  
pp. 1197-1204 ◽  
Author(s):  
H IIJIMA ◽  
I TAKAHASHI ◽  
T HIROI ◽  
M SHIMAOKA ◽  
S KAWANO ◽  
...  
Keyword(s):  
T Cells ◽  
Cholera Toxin ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B

scholarly journals 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

2006 ◽  
Vol 75 (1) ◽  
pp. 306-313 ◽  
Author(s):  
R. Plaza ◽  
J. L. Rodriguez-Sanchez ◽  
C. Juarez
Keyword(s):  
T Cells ◽  
Gamma Interferon ◽  
Staphylococcal Enterotoxin ◽  
Receptor Expression ◽  
Protective Mechanism ◽  
Staphylococcal Enterotoxin B ◽  
Selective Blockade ◽  
Stat1 Signaling ◽  
Ifn Γ ◽  
Enterotoxin B

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-γ) response is deeply affected in both extremes. The implication of IFN-γ 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-γ 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-γ serum release 72 h after priming. However, at this time, a selective blockade of IFN-γ/STAT1 signaling develops in spleen cells, correlating with a lack of expression of the IFN-γ 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-γ production during the Th1 effector response. This blockade may also have consequences on switching towards a suppressor phenotype with chronic exposure to the superantigen.

Role of Staphylococcal Enterotoxin B on the Differentiation of Regulatory T Cells in Nasal Polyposis

2014 ◽  
Vol 28 (1) ◽  
pp. e17-e24 ◽  
Author(s):  
Soo-Na Cho ◽  
Chang-Hwa Song ◽  
Jun Jin ◽  
Sung Ha Kim ◽  
Ki-Sang Rha ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Nasal Polyposis ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B
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