Abstract
Atopic dermatitis is characterized by a reduced capacity of barrier-free functions and the development of damaging inflammation II. type. Alarmins, which are formed or released by activated or damaged keratinocytes, play a crucial role in its initiation.
Among the alarms II. types include IL-25, TSLP, and especially IL-33. The IL-33 alarmin can be structurally classified into the interleukin-1 family.
However, it has the unique ability to act as a transcription factor. Alarmine II. type stimulate dendritic cells and ILC-2 cells.
The result is the development and amplification of damaging inflammation. The role of IL-33 not only in the pathophysiology of inflammation II. type is very complex.
It significantly regulates a number of fundamental biological processes of the body. IL-33 could become a target for therapeutic interventions in the future.