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English: Figure 1. Model of the role of mucosal lamina professional and non professional APCs in SE associated Gastro-Intestinal (GI) inflammatory injury. GI inflammatory injury during staphylococcal enterotoxigenic disease is mediated mostly through the SE superantigenic effect on MHC class II expressing mucosal professional (macrophages and dendritic cells, DC) and non professional (such as myofibroblasts) APCs and TCR expressing CD4+ T cells. SE can cross the intestinal epithelial barrier in intact form and bind to class II MHC molecules that expressed on subepithelial myofibroblast. These processes will lead to a strong production of the proinflammatory cytokines and chemokines, including IL-6, IL-8 and MCP-1. The last one may leads to the increased chemotaxis of professional immune cells (CD4+ T cells, Macrophages, DC) from gut associated lymphoid tissue (GALT) to the site of SE associated inflammation in GI mucosa. Those MHC class II:SEs:TCR interactions may in turn result in hyperactivation of the APCs and the T cells leading to the excessive proliferation of T cells and the uncontrolled burst of various proinflammatory cytokines and chemokines causing the superantigen-mediated acute inflammation and shock.