In the last decades the knowledge on pathogenetic mechanisms of allergic diseases extraordinarily improved with relevant clinical outputs. From the '90yrs we know that Th2 cells are essential for allergic inflammation, since they produce type 2 cytokines, recognise allergens, induce IgE switch on B cells and recruit mastcells and eosinophils into tissues for maintaining the flogosis. Recently a new subset of innate immunity (ILC2) have been shown to amplify the allergic inflammation. The chronicity of respiratory allergy is characterised by tissue signals which address T cell to a "Th2 high"- (ILC2/Th2 responses) or a "Th2 low" (ILC3/Th17 responses) endotype, with a BAL prevalence of eosinophils or neutrophils, respectively. This double response is essentially due to T effector cell plasticity, modulated by microenvironmental signals. The discovery of new endotypes, diagnosed by selective biomarkers and cured by biological agents, will open the era of personalised medicine also for respiratory allergic disorders.