Figure 6: Diagrammatic representation of possible mechanistic pathway for the induction of EGID. Allergens (Aero- or food-) procured by antigen presenting cells (APCs) are offered to the conventional (CD4+ T cells) and non-conventional T cells (iNKT cells). Based on our earlier reports and presented information in the review, we propose that both conventional CD4 T cells and non-conventional iNKT cells generate eosinophil active Th2 cytokines like IL-4, IL-5, IL-13.The iNKT cells require IL-15 and IL-18 for survival, proliferation and activation. The antigen presenting cells may be the major source of IL-15 and IL-18 to activate iNKT cells to initiate the disease process in a number of gastrointestinal disorders like EoE, EGE and EC. IL- 18 is a unique cytokine that has a role in a number of allergic diseases and recent publication indicates that IL-18 overexpression in the tissues promotes eosinophilic inflammation and tissue remodeling through the induction of TGFα/β. Our earlier publications and evidences presented in this review indicate that STAT5 and STAT6 regulate the activation of CD4+ T and iNKT cells, respectively. Interestingly, the role of eosinophil active Th2 cytokines and chemokines (eotaxins-1, and eotaxin-3) in gastrointestinal epithelial mucosa is critical in the accumulation of eosinophils into the esophagus (via eotaxin-3 involvement) and in the intestine and colon (via Eotaxin-1 involvement), respectively, which promotes EGID.