Table 3.

The main finding about the role of ILC2s in atopic dermatitis.

Authors	Year	Study Characteristics
Nishikawa et al. [67]	2021	A mouse model using transgenic binary mice that are constitutively deficient in conventional dendritic cells (cDCs) demonstrated that congenital cDCs deficiency not only exacerbated atopic dermatitis (AD)-related inflammation but also resulted in immune alterations as the composition and function of the cells increased granulocytes and group 2 innate lymphoid cells (ILC2s).
Früh et al. [66]	2020	In a canine model, levated frequencies and numbers of T-helper 2 cells but not ILC2s in peripheral blood were associated with chronic canine atopy.
Imai et al. [78]	2019	In a mouse model, ILC2 cells were depleted in IL33tg mice via bone marrow transplantation; in these mice, the development of inflammation was almost completely suppressed, demonstrating the central role of ILC2s in immune processes.
Salimi et al. [70]	2013	The binding of E-cadherin to human ILC2s dramatically inhibited interleukin (IL)-5 and IL-13 release. In the absence of E-cadherin, which is characteristic of filaggrin insufficiency and feature of AD, ILC2s resulted in increased production of type 2 cytokines.
Salimi et al. [74]	2015	The expression of NKp30 ILC2s ex vivo and on cultured ILC2s and the interaction with its ligand B7-H6 induced the production of type 2 cytokines in AD.
Baek et al. [85]	2017	In a mouse model, immune tolerance was induced by oral administration of ovalbumin with subsequent epicutaneous sensitization by repeated application of ovalbumin. The induction of oral tolerance resulted in a reduction in the inflammatory response through the inhibition of ILC2 levels.
Perrone Sibilia et al. [84]	2019	Chronic infection with Toxoplasma gondii appeared to prevent the development of atopic dermatitis through a reduced susceptibility that appeared to result from changes in the type II innate immune response, with reductions in IL-4, IL-5, and ILC2s.
Lee et al. [82]	2021	Celastrol decreased the levels of thymic stromal lymphopoietin (TSLP), ILC2s, and T-helper 2-cytokines in AD lesions of house dust mite-stimulated NC/Nga mice.
Mashiko et al. [68]	2017	AD lesional skin, but not psoriasis skin, was infiltrated by increased numbers of basophils, which produced IL-4,T-helper 2 cells and ILC2s.
Schwartz et al. [79]	2019	ILC2 deficiency did not improve AD in Flgft/ft mice, which was also independent of IL-4, IL-5, IL-9, IL-13, IL-17A, and IL-22, but required the signaling of IL-1β and IL-1R1, which therefore, also play a fundamental role in the development of inflammation.
Natsume et al. [83]	2020	A study comparing the anti-itch effect of xanthophyll with tacrolimus observed that the former significantly reduced symptoms compared to the latter through the presence of ILCreg suppressing the immune response.
Hardman et al. [73]	2017	In a human AD-based model, TSLP-induced ILC2s expressed Cluster of Differentiation 1a (CD1a), which, in turn, activated TH lymphocytes. In addition, ILC2s presented endogenous lipid antigens to CD1a-reactive T cells.