Fig. 1

Mechanism of asthma development. The physiopathological mechanism of asthma involves three complex currently mechanisms: 1. The polarization of Th2 response with the production of cytokines such as IL-4, IL5 and IL-13, participation of sIgE, mast cell degranulation and predominance of eosinophils (classic atopic asthma); 2. Predominant participation of Th17 response, production of IL-17A; IL-17 F; IL-21 and IL-22 cytokines and the presence of neutrophils (probable mechanism of non-atopic asthma or increasing severity of atopic asthma); 3. Through the innate immunity activation where two main actions could be involved, the release of cytokines from epithelial cells, TSLP and IL-33, and the interaction between iNKTs and ILCs cells. The TSLP acts on the activation of dendritic cells and induction of Th2 response, and differentiation of T cells in Th17 profile. The IL-33 acts on the interaction between iNKTs and ILCs, but also acts enriching Th2-type cells. Evidence that suggests the FOXP3 transcription factor, which is constitutively expressed in CD4 + CD25 + Foxp3 + regulatory T cells (Treg) is critical for the maintenance of homeostasis and immune systemand alsoare responsible for the suppression of the Th2 and Th17 responses. DC = dendritic cells; sIgE = specificIgE; TLSP = thymic stromal lymphopoietin; iNKTs = invariant natural killer T; ILC2s = type 2innate lymphoid cells