IL1A and Alzheimer disease: These toxins function as superantigens (SAgs) [42] to activate T cell clones, resulting in substances capable of mounting an extremely strong immune response, which subsequently triggers IgE-mediated mast cell degranulation and elevates Th2 cytokines [43]; moreover, they bind to human leukocyte antigen-DR on Langerhans cells and macrophages to stimulate the production of IL-1, TNF-α, and IL-12, thus contributing to the exacerbation and recurrence of AD [43].