Galle-Treger L, Hurrell BP, Lewis G, et al. - Since a high amount of Th2 cytokines are secreted by group 2 innate lymphoid cells (ILC2s) in allergic asthma, adding to the development of airway hyperreactivity (AHR), researchers determined how ILC2s effector functions and metabolic balance would be influenced by autophagy deficiency. They used autophagy deficient mice in this investigation. Findings revealed extensive use of autophagy by activated ILC2s for the purpose of sustaining their homeostasis and effector functions. Reduced cytokine secretion and enhanced apoptosis resulting from the deletion of the critical autophagy gene Atg5 were also observed. In transcriptomic and metabolite analyses, an impairment of the ability of ILC2s to utilize fatty acid oxidation as well as the striking promotion of glycolysis, both were observed as consequences of lack of autophagy among ILC2s. They noted impaired homeostasis and Th2 cytokine generation which was induced by this shift of fuel dependency, this ultimately led to inhibition of the development of ILC2-mediated AHR. Overall, experts viewed modulation of fuel dependency by autophagy as a potentially novel therapeutic strategy to target ILC2 dependent inflammation.