Table 4.

The main finding about the potential therapeutic role of ILC2s in melanoma, AD and cutaneous type 2 inflammation.

Authors	Target	Disease	Immunological Mechanism
Okuyama et al. [38]	IL-33/ST2 interaction	melanoma	Group 2 innate lymphoid cells (ILC2s), once stimulated by interleukin (IL)-33 after binding with their ST2 receptor, play a tumor role activating CD8+ T-cell expression and infiltration into the tumor and inducing an unfavorable tumor environment.
Jacquelot et al. [36]	PD1	melanoma	Inhibition of programmed cell death protein (PD-1) results in increased total ILC2s number. High ILC2s infiltration in human melanoma is associated with a good clinical prognosis.
Wagner et al. [37]	Lactic acid	melanoma	Acid lactic inhibits ILC2 proliferation and cytokine production, exerting immunosuppressive activity against ILC2s. Conversely. in knockdown lactate dehydrogenase A B16F10 melanomas (LDHAlow), the number of intratumoral ILC2s increased proportionally.
Ricardo-Gonzalez et al. [57]	IL-18	Cutaneous type 2 inflammation	-Subpopulations of ILC2-expressing receptors for IL-18 are responsible for the most severe forms of allergic skin inflammation; -Increased levels of IL-18 correlate with the severity of dermatitis; -IL-18 and IL-33 action on ILC2s would appear to be closely related.
Numazaki et al. [64]	TSLP	Cutaneous inflammation	In vitro study demonstrated that monoclonal anti-thymic stromal lymphopoietin (TSLP) receptor antibodies managed to reduce both type 2 and non-type 2 inflammation.
Salimi et al. [74]	NKp30	AD	Cultured ILC2s subset expressing NKp30, after interaction with its activator ligand B7-H6, rapidly produce type 2 cytokines.