Abstract
There are multiple proinflammatory pathways in the pathogenesis of asthma. These include both innate and adaptive inflammation, in addition to inflammatory and physiologic responses mediated by eicosanoids. An important component of the innate allergic immune response is ILC2 activated by interleukin (IL)-33, thymic stromal lymphopoietin, and IL-25 to produce IL-5 and IL-13. In terms of the adaptive T-lymphocyte immunity, CD4+ Th2 and IL-17-producing cells are critical in the inflammatory responses in asthma. Last, eicosanoids involved in asthma pathogenesis include prostaglandin D(2) and the cysteinyl leukotrienes that promote smooth muscle constriction and inflammation that propagate allergic responses.