To investigate the driving force behind the increase of ILCs in atopic dermatitis (AD) skin, we numerically and phenotypically compared ILC (sub)populations in the blood of AD patients and healthy controls (HC). 
For this purpose, peripheral blood mononuclear cells (PBMCs) were isolated from clinically active AD patients (n=19) and age-matched (35.5 ± 0.1 years) healthy individuals (n=17), immunostained with a panel of subset-characterising antibodies and analysed with a BD FACS Aria III sorter. Total ILCs were defined as viable CD45+, CD3-, Lin-, CD127+, CD161+ mononuclear cells and expressed as percent of CD45+ cells (mean ± SEM). Subpopulations of total ILCs were defined as follows: ILC1 (CD117-, CRTH2-), ILC2 (CRTH2+), and ILC3 (CD117+, CRTH2-).
Results obtained show that the amount of total ILCs among PBMCs is significantly lower in AD patients than in healthy individuals (AD: 0.025 ± 0.004; HC: 0.044 ± 0.006, p = 0.006). As far as ILC subsets are concerned, we encountered an altered distribution (percentage of total ILCs, mean ± SEM) in AD patients vs healthy controls with a relative increase in ILC1 and a reduction of ILC2 in the former group (ILC1: AD: 26.53 ± 4.63; HC: 12 ± 2.30; p = 0.0104; ILC2: AD: 20.56 ± 2.78; HC: 34.32 ± 3.66; p = 0.0046). No significant difference was observed for ILC3 in the blood of AD patients and HC.
Our data support the concept that the reported increase of ILCs, particularly ILC2, in AD skin is at least partly due to emigration from blood and that this pathogenic loop could be a potential pharmacologic target.

Innate lymphoid cells (ILCs) in healthy and atopic blood