1,25(OH)VitD3 inhibited IL33 and Ror-alpha in the airways
We then asked if ILC2 were upregulated in our model of airway tolerance after intranasal treatment with VitD3 and allergen challenge(Fig 4a). 24
Here we found that, intranasal delivery of VitD3, reduced Amphiregulin (AREG), which is a member of the epidermal growth factor family(Fig 4b), as well as IL-33, an alarmin and ligand of ST2, a receptor on Innate lymphoid cells6 (Fig 4c ). Intranasal delivery of VitD3 did not regulate the ILC2 markers ST2 nor ICOS (Fig 4 d, e) but reduced Ror-alpha, an ILC2 signature transcription factor (Fig 4f)25. Thus airway tolerance induced by VitD3 and allergen given intranasally did not suppress completely ILC2 as confirmed by residual ILC2 cytokine IL-5 and IL-13 in the airways of treated mice (Fig 4 g,h) .