Figure 4.

Redistribution of innate lymphoid cells (ILCs) in obesity: a link with asthma? A hypothetic mechanism. At baseline ILC2 and ILC3 are decreased in adipose tissue (AT) but present in lung tissue from obese mice, potentially through redistribution of ILCs from the AT to the lung under the effect of interleukin‐1β (IL‐1β). This leads to a small infiltration of eosinophils in the lung tissue of obese mice. In the context of allergic airway inflammation, there is a further increase in ILC2 and ILC3 at the lung level, that might originate partly from the adipose tissue but also putatively from the bone marrow and from circulating progenitors attracted by the production of IL‐33 and IL‐1β induced by allergen challenge. This increase drives further accumulation of eosinophils, activation of Th2 and Th17 cells potentially through antigen presentation, and aggravation of the features of asthma.