The immune system is comprised of the innate immune system, which acts as a rapid, nonspecific first line of defense against pathogens and environmental insults, and the adaptive immune system, which acts with specificity to provide a more robust and targeted response.1
Type 2 inflammation (T2I) is driven by both the adaptive and innate arms of the immune system.1 In a typical type 2 immune response, the epithelium releases alarmins IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) on the allergen or environmental insult, initiating the type 2 response.2,3
These factors signal innate cells, including basophils, mast cells, and type 2 innate lymphoid cells (ILC2), to produce and release the type 2 cytokines IL-4, IL-5, and IL-13. IL-4 serves as a master regulator, promoting the differentiation of naïve CD4+ T cells into Th2 cells that further amplify the response by producing additional IL-4, IL-5, and IL-13 cytokines, creating a self-amplifying inflammatory cascade.4
IL-4 and IL-13 share several overlapping functions due to their common receptor complex (IL-4Rα), including: 4
IL-5 specifically drives eosinophil differentiation, maturation, and survival in the bone marrow, while also supporting the development of other type 2 cells, including mast cells and basophils.4
The type 2 inflammatory response induces several characteristic tissue changes: 4
