Ken Arae

TL;DR: It is found that IL-1, but not IL-33, played a substantial role in induction of T cell-mediated type IV hypersensitivity such as contact and delayed-type hypersensitivity and autoimmune diseases such as experimental autoimmune encephalomyelitis andIL-33 was important for innate-type mucosal immunity in the lungs and gut.

TL;DR: A unique anti-inflammatory pathway is identified that can limit induction of innate-type allergic airway inflammation mediated by NH cells.

TL;DR: A unique immune regulatory and anti-inflammatory pathway is identified by which RA converts ILC2s to ILCregs, which expresses a regulatory T cell-like signature with expression of IL-10, cytotoxic T lymphocyte-associated protein 4, and CD25.

TL;DR: Current knowledge regarding the roles of IL‐33 in the functions of various cell types and the pathogenesis of allergy suggests that it acts as an alarmin, like IL‐1α and high‐mobility group box chromosomal protein‐1 (HMGB‐1).

TL;DR: Airway structural cell- derived IL-25—rather than Th17 cell-derived IL- 17A and IL-17F—is responsible for induction of local inflammation by promoting activation of lung epithelial cells and eosinophils in the elicitation phase of Th2-type/eosinophile airway inflammation.