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Superantigen Enhancement of Specific Immunity: Antibody Production and Signaling Pathways¹

Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611

Superantigens are microbial proteins that induce massive activation, proliferation, and cytokine production by CD4⁺ T cells via specific V elements on the TCR. In this study we examine superantigen enhancement of Ag-specific CD4⁺ T cell activity for humoral B cell responses to T-dependent Ags BSA and HIV gp120 envelope, type I T-independent Ag LPS, and type II T-independent Ag pneumococcal polysaccharides. Injection of BSA followed by a combination of superantigens staphylococcal enterotoxin A and staphylococcal enterotoxin B (SEB) 7 days later enhanced the anti-BSA Ab response in mice 4-fold as compared with mice given BSA alone. The anti-gp120 response was enhanced 3-fold by superantigens. The type II T-independent Ag pneumococcal polysaccharide response was enhanced 2.3-fold by superantigens, whereas no effect was observed on the response to the type I T-independent Ag LPS. The superantigen effect was completely blocked by the CD4⁺ T cell inhibitory cytokine IL-10. SEB-stimulated human CD4⁺ T cells were examined to determine the role of the mitogen-activated protein (MAP) kinase signal transduction pathway in superantigen activation of T cells. Inhibitors of the mitogen pathway of MAP kinase blocked SEB-induced proliferation and IFN- production, while an inhibitor of the p38 stress pathway had no effect. Consistent with this, SEB activated extracellular signal-regulated kinase/MAP kinase as well as MAP kinase-interacting kinase, a kinase that phosphorylates eIF4E, which is an important component of the eukaryotic protein synthesis initiation complex. Both kinases were inhibited by IL-10. Thus, superantigens enhance humoral immunity via Ag-specific CD4⁺ T cells involving the stress-independent pathway of MAP kinase.

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