scholarly journals The role of IL-4 in the staphylococcal enterotoxin B-triggered immune response: increased susceptibility to shock and deletion of CD8Vβ8+ T cells in IL-4 knockout mice

Author(s):  
Luiz Stark Aroeira ◽  
Carlos Martínez-A.
1992 ◽  
Vol 176 (2) ◽  
pp. 575-579 ◽  
Author(s):  
W T Lee ◽  
E S Vitetta

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.


2001 ◽  
Vol 69 (9) ◽  
pp. 5949-5952 ◽  
Author(s):  
Fanny N. Lauw ◽  
Sandrine Florquin ◽  
Peter Speelman ◽  
Sander J. H. van Deventer ◽  
Tom van der Poll

ABSTRACT In the present study, the roles of interleukin 12 (IL-12) and IL-18 and their possible interaction during superantigen-induced responses were studied by injection of staphylococcal enterotoxin B (SEB) into mice. These data suggest that the role of IL-12 in SEB-induced responses is limited to sustaining gamma interferon release by an IL-18-independent mechanism.


2014 ◽  
Vol 28 (1) ◽  
pp. e17-e24 ◽  
Author(s):  
Soo-Na Cho ◽  
Chang-Hwa Song ◽  
Jun Jin ◽  
Sung Ha Kim ◽  
Ki-Sang Rha ◽  
...  

2005 ◽  
Vol 12 (9) ◽  
pp. 1119-1122 ◽  
Author(s):  
Govindarajan Rajagopalan ◽  
Manisha Singh ◽  
Moon M. Sen ◽  
Narayana S. Murali ◽  
Karl A. Nath ◽  
...  

ABSTRACT Endogenous superantigen-mediated thymic negative selection resulted in a paucity of mature T cells bearing T-cell receptor (TCR) Vβ8 in the periphery. Consequently, the magnitude of immune response to exogenous superantigen staphylococcal enterotoxin B, which activates TCR Vβ8+ T cells, was significantly reduced and conferred protection from superantigen-induced mortality.


2000 ◽  
Vol 105 (4) ◽  
pp. 820-826 ◽  
Author(s):  
Lone Skov ◽  
Jeanett V. Olsen ◽  
Ralph Giorno ◽  
Patrick M. Schlievert ◽  
Ole Baadsgaard ◽  
...  

2006 ◽  
Vol 117 (2) ◽  
pp. S62
Author(s):  
S.K. Mathur ◽  
E.A. Durocher ◽  
L. Liu ◽  
E.A.B. Kelly ◽  
J.B. Sedgwick ◽  
...  

1996 ◽  
Vol 183 (6) ◽  
pp. 2481-2488 ◽  
Author(s):  
H W Mittrücker ◽  
A Shahinian ◽  
D Bouchard ◽  
T M Kündig ◽  
T W Mak

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.


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