Fig. 2.

Immune cells and the inflammatory cascade in asthma. Initial exposure(s) to allergen leads to the activation of allergen-specific Th2 cells and IgE synthesis (sensitisation). Subsequent allergen exposures cause inflammatory-cell recruitment, activation and mediator release. IgE-sensitised mast cells expressing the high affinity IgE receptor (FcɛRI) degranulate, releasing both pre-formed and newly synthesized mediators including histamine, leukotrienes and cytokines, which promote vascular permeability, smooth muscle contraction and mucus production. Chemokines released by inflammatory and resident cells direct recruitment of inflammatory cells characterised eosinophils and Th2 cells. Eosinophils release an array of pro-inflammatory mediators, including leukotrienes and basic proteins and mediators such as, IL-5. Key: APC, antigen-presenting cell; ASM, airway smooth muscle; EpC, epithelial cell; GM-CSF, granulocyte monocyte colony stimulating factor; MHC, major histocompatibility; TCR, T cell receptor; TSLP, thymic stromal lymphopoietin.