After exposure to antigens, naive CD4+ (cluster of differentiation 4) T cells can be differentiated in different subsets of T helper (Th) cells (Th1, Th2, Th9, Th17, Th22, Tfh) and induced suppressive regulatory T cells characterized by different cytokine expression patterns, transcription factors and other surface markers, which will orchestrate adaptive and innate immune responses to these stimuli. Th2 cells are central players in all the various forms of Immunoglobulin E (IgE)-associated allergic diseases and are thus regarded as the most dominant T cell subset sustaining the allergic response. Upon antigen uptake and processing by antigen-presenting cells, CD4+ T cells are polarized towards a Th2 phenotype, leading to the expression of Th2 cell-associated cytokines such as Interleukin (IL)-4, -5, -9, -13, switching B cell response toward IgE production (sensitization or early phase). Allergen-specific IgE bind to a high-affinity receptor (FcεRI) of innate immune cells including basophils and mast cells, triggering the release of anaphylactogenic mediators (cytokines, chemokines, histamine, heparin, serotonin and proteases) responsible for inflammatory cell recruitment and allergic symptoms (effector or late phase). Identifying networks of genes expressed in resting and activated Th2 cells from allergic patients would help distinguish gene candidates predicting immune tolerance to allergens.