Study The The Generol Mechanisms Of The Inhibition Effectors Of SEB As Superantigen Act On Mice

When pathogenic microorganisms invade into organism, how does these pathogenic microorganisms escape form the immuno-system and successfully settle down in the organim is a key issue to understand the mechanism of infect and the pathopoiesis of pathogenic microorganisms. Among all the pathopoiesis agents that release from pathogenic microorganisms, superantigens sever very important roles in immunodeficiency, for they can directily binding also MHC classâ…¡molecules and TCR receptors but do not request angtigen presentation prosess. Superantigen can activate a great number of immuno-cells causes a verity of effects, including ctyokins release, cellsurance molecules express and so on, but how pathopoiesis agents utilize these superantigens to avoid the immunosystem attack is not clear yet.Administration of bacterial superantigen results in clonal activation of T cells followed by a state of hyporesponsiveness to subsequent antigen stimulation. Using a coculture system, we showed that the splenocytes from staphylococcal enterotoxin B (SEB)-injected BALB/c mice suppressed the proliferative response of naive syngeneic splenocytes to SEB stimulation, and T cells mediated the suppressive activity. Detected by FACScan, we found an increased CD4~+CD25~+ T cell voluem in SEB-primed effector cells Vis saline-primed eddector cells. The IL-2 levels in culture supernatants were low with the presence of SEB-primed effector cells. However, addition of IL-2 to the cocultures only partially reversed the inhibitory effect. The addition of anti-CD28 mAb could reverse the suppressive effect on naive cell proliferation in the coculture experiments. Compsite all the results of our experimental, we infer that the intensity between TCR/MHC, the activation of regulatory CD4~+CD25~+T lymphocyte thus cause the inhibition effects and the constimulatory signal form CD28 molecule may sever significant roles in SEB-primed T lymphocyte to generate immunosuppressive activity.Taken together, when SEB is used as a stimulator in vivo, both MHC molecule and CD28 costimulation are required for the induction of the regulatory cells bearing suppressive activity, all these may serve at least in part the mechanisms of SEB-induced hyporesponsiveness.