Autophagy has been shown to play a critical role in kidney maintenance, disease, and aging. In this study, the authors identified a novel mechanism by which IFN-γ activates autophagy in human kidney epithelial cells. They found that IFN-γ promoted tryptophan depletion, activated the eIF2α kinase general control nonderepressible-2 (GCN2), and led to an increase in the autophagic flux. The use of an antibody array was instrumental in determining that the noted increase in autophagy downregulated the secretion of inflammatory cytokines and growth factors by human kidney epithelial cells. Overall, their results provided insights into how autophagy regulates immune functions in response to IFN-γ.
Fougeray S., Mami I., Bertho G., et al. Tryptophan depletion and the kinase GCN2 mediate IFN-γ-induced autophagy. J Immunol. 2012 Sep 15;189(6):2954-64. doi: 10.4049/jimmunol.1201214.