IGHE and Autoimmunity: Current evidence shows that the activation of mast cells rich in high-affinity receptors followed by rapid degranulation, the development of autoimmunity (type I, defined by IgE antibodies against autoantigens or type 2b, defined by IgG anti-IgE and IgG anti-FcεRI autoantibodies), and the alteration of cytokine–chemokine networks are intensely debated pathogenetic mechanisms in CSU.