Figure 1

ILC1, ILC2 and ILC3 interactions in human skin. ILC1s express CD161. ILC2s express IL-17RB, ST2, CRTH2, TSLPR and an inhibitory receptor KLRG1. In homeostatic conditions, the expression of adhesion molecule E-cadherin on normal human keratinocytes inhibits the activation of ILC2s. NKp44⁻ ILC3s are the main subset of ILC3 in healthy skin. ILC2s are enriched in atopic dermatitis lesions and show higher expression of ST2, IL-17RB and TSLP-R, probably an activated phenotype. They express IL-13, IL-5, and IL-4 in response to IL-33, IL-25 and TSLP produced by keratinocytes and PGD2 released by mast cells and other cells. Concurrently, the diminished expression of E-cadherin on keratinocytes is a novel mechanism of sensing a dysfunctional barrier. The frequency of ILC1 and ILC3 in AD lesions are similar to healthy skin. The frequency of NKp44⁺ ILC3s is increased in psoriatic skin lesions. They produce IL-22 when stimulated with IL-23.