IL33 and Alzheimer disease: Imai's team276 reported that after constructing IL‐33‐overexpressing transgenic mice, basophils in IL‐33‐overexpressing transgenic mice accumulated in the AD lesion areas of the mice and that when basophils and type 2 innate lymphocytes (ILC2s) were depleted, the development of AD‐like inflammation was almost completely suppressed in IL‐33 transgenic mice.