Nick Pitman

TL;DR: IL-33 is host-protective against helminth infection and reduces atherosclerosis by promoting TH2-type immune responses but can also promote the pathogenesis of asthma by expanding TH2 cells and mediate joint inflammation, atopic dermatitis and anaphylaxis by mast cell activation.

TL;DR: It is demonstrated here that IL-33/ST2 plays a significant role in the amplification of AAM polarization and chemokine production which contribute to innate and Ag-induced airway inflammation.

TL;DR: It is demonstrated that IL- 33 is a critical proinflammatory cytokine for inflammatory joint disease that integrates fibroblast activation with downstream immune activation mainly via an IL-33-driven, mast-cell-dependent pathway and represents a therapeutic target for RA.

TL;DR: It is demonstrated here that, in the presence of Ag, IL-33 induces IL-5-producing T cells and promotes airway inflammation independent of IL-4.

TL;DR: The novel cytokine interleukin-33 (IL-33) potently induces anaphylactic shock in mice and is associated with the symptom in humans, revealing a hitherto unrecognized pathophysiological role of IL-33 and suggesting that IL- 33 may be a potential therapeutic target for anaphlyaxis, a disease of considerable unmet medical need.