How are TH2-type immune responses initiated and amplified?

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Abstract
GATA-binding protein 3 (GATA3) expression and signal transducer and activator of transcription 5 (STAT5) activation are two key events for TH2 cell differentiation in vitro and possibly in vivo. Epithelial cells, dendritic cells and basophils are responsible for sensing allergens and helminth products and thus initiate TH2-type immune responses in vivo. Epithelial cells produce the TH2-promoting cytokines thymic stromal lymphopoietin (TSLP), interleukin-25 (IL-25) and IL-33, and basophils produce IL-4, TSLP and IL-25 during the initiation stage of TH2 cell development. These cytokines may have important roles in inducing TH2-type responses, but the relative importance of each cytokine differs among individual models of TH2 cell-associated diseases. Both dendritic cells and basophils can serve as TH2-inducing antigen-presenting cells. Although basophils are crucial for some TH2-type responses, they are dispensable in other models where dendritic cells or other potential antigen-presenting cells are involved. IL-25 and IL-33 responsive non-B non-T cells produce TH2-associted cytokines, including IL-5 and IL-13, following IL-25 or IL-33 stimulation. These cells can be thought to be innate effector cells during TH2-type responses. IL-4, TSLP, IL-25 and IL-33 are also involved in the amplification of the TH2-type responses by affecting several cell types.