Abstract
Staphylococcus aureus enterotoxins have immunomodulatory properties. In this study, we show that Staphylococcal enterotoxin A (SEA) induces a strong proliferative response in a murine T cell clone independent of MHC class II bearing cells. SEA stimulation also induces a state of hypo-responsiveness (anergy). We characterized the components of the T cell receptor (TCR) during induction of anergy by SEA. Most interestingly, TCR zeta chain phosphorylation was absent under SEA anergizing conditions, which suggests an uncoupling of zeta chain function. We characterize here a model system for studying anergy in the absence of confounding costimulatory signals.
Highlights
Staphylococcus aureus enterotoxins have been implicated in a number of acute and chronic human diseases including food poisoning, tampon related toxic shock, scalded skin syndrome, Kawasaki syndrome, and shock [1,2,3]
We wanted to determine the capacity of A.E7 T cells to proliferate in response to Staphylococcal enterotoxin A (SEA) in the presence or absence of syngeneic class II-bearing antigen presenting cells (APC)
20-fold higher concentration of SEA. These results are consistent with previous results reported from this laboratory [18,19], and others [26,27], which have shown that T cells may exhibit a proliferative response to superantigen in the absence of intact APCs
Summary
Staphylococcus aureus enterotoxins have been implicated in a number of acute and chronic human diseases including food poisoning, tampon related toxic shock, scalded skin syndrome, Kawasaki syndrome, and shock [1,2,3]. Kinases, such as, p56lck, p59fyn, and zap-70 are brought in close proximity of the TCR by CD4 and other costimulatory molecules and are rapidly phosphorylated following TCR stimulation [5,6,7,8,9,10,11] The results of these signaling events are the production of IL-2, the autocrine IL-2-induced activation of the IL-2 receptor complex, and clonal expansion of the T cell through proliferation. We report an in vitro model of anergy using superantigen in the absence of MHC class II bearing cells to examine the proximal TCR signaling events that lead to the induction of an anergic phenotype The advantage of this experimental system is that T cell clonal anergy is induced under highly simplified conditions where there are no complicating signals contributed by the APCs. The purpose of the present studies was to characterize the proximal signaling events following induction of anergy under these conditions. These studies demonstrate that the failure to hyper-phosphorylate zeta chain is mediated directly by the ligation of the TCR by superantigen
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