Impaired T Cell Proliferation and Zeta Chain Phosphorylation after Stimulation with Staphylococcal Enterotoxin-B in Hemodialysis Patients

2004 ◽  
Vol 96 (1) ◽  
pp. c15-c20 ◽  
Author(s):  
Theodoros Eleftheriadis ◽  
Konstantinos Papazisis ◽  
Alexandros Kortsaris ◽  
Georgios Vayonas ◽  
Sultana Voyatzi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Hemodialysis Patients ◽  
Staphylococcal Enterotoxin ◽  
T Cell Proliferation ◽  
Staphylococcal Enterotoxin B ◽  
Zeta Chain ◽  
Enterotoxin B

scholarly journals Anti-Vβ8 antibodies induce and maintain staphylococcal enterotoxin B-triggered Vβ8+ T cell anergy

1999 ◽  
Vol 29 (2) ◽  
pp. 437-445 ◽  
Author(s):  
Luiz Stark Aroeira ◽  
Concepción G. Mouton ◽  
José L. Toran ◽  
Elizabeth Sally Ward ◽  
Carlos Martínez-A.
Keyword(s):  
T Cell ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
T Cell Anergy ◽  
Enterotoxin B ◽  
Cell Anergy

scholarly journals CD4 + T‐cell‐mediated cytotoxicity against staphylococcal enterotoxin B‐pulsed synovial cells

Immunology ◽  
1998 ◽  
Vol 95 (1) ◽  
pp. 38-46 ◽  
Author(s):  
KAWAKAMI ◽  
MATSUOKA ◽  
TSUBOI ◽  
URAYAMA ◽  
NAKASHIMA ◽  
...  
Keyword(s):  
T Cell ◽  
Staphylococcal Enterotoxin ◽  
Cd4 T Cell ◽  
Staphylococcal Enterotoxin B ◽  
Synovial Cells ◽  
Enterotoxin B

Staphylococcal enterotoxin B induces fever, brain c-Fos expression, and serum corticosterone in rats

2001 ◽  
Vol 280 (5) ◽  
pp. R1434-R1439 ◽  
Author(s):  
Lisa E. Goehler ◽  
Ron P. A. Gaykema ◽  
Michael K. Hansen ◽  
Jayme L. Kleiner ◽  
Steven F. Maier ◽  
...  
Keyword(s):  
T Cell ◽  
Host Defense ◽  
Intraperitoneal Injection ◽  
Defense Responses ◽  
Plasma Corticosterone ◽  
Significant Rise ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B ◽  
Fos Expression

The paraventricular nucleus of the hypothalamus (PVH) occupies a pivotal point within the network of brain nuclei coordinating critical host-defense responses. In mice, T cell-dependent immune stimuli, including the bacterial superantigen staphylococcal enterotoxin B (SEB), can activate the PVH. To determine whether T cell-dependent immune stimuli activate the PVH in rats, we assessed plasma corticosterone (Cort) levels, fever responses, and c-Fos expression in the PVH in animals treated with intraperitoneal injections of SEB. In animals with previously implanted abdominal thermisters, intraperitoneal injection of 1 mg/kg SEB resulted in a significant rise in body temperature, with a latency of 3.5–4 h. In separate animals, intraperitoneal injection of 1 mg/kg SEB resulted in a significant elevation of plasma Cort and induced c-Fos expression in parvocellular neurons within the PVH. These results support the idea that T cell-dependent immune stimuli activate brain pathways mediating host-defense responses such as fever and neuroendocrine changes.

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.

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