Yano, TamakiMita, ShizukaOhmori, HirokoOshima, YoshiteruFujimoto, YukariUeda, RyuTakada, HaruhikoGoldman, William E.Fukase, KoichiSilverman, NealYoshimori, TamotsuKurata, Shoichiro2022-08-232022-08-232008-07-082009-12-15Nat Immunol. 2008 Aug;9(8):908-16. Epub 2008 Jul 6. <a href="http://dx.doi.org/10.1038/ni.1634">Link to article on publisher's site</a>1529-2916 (Electronic)10.1038/ni.163418604211https://hdl.handle.net/20.500.14038/34981Autophagy, an evolutionally conserved homeostatic process for catabolizing cytoplasmic components, has been linked to the elimination of intracellular pathogens during mammalian innate immune responses. However, the mechanisms underlying cytoplasmic infection-induced autophagy and the function of autophagy in host survival after infection with intracellular pathogens remain unknown. Here we report that in drosophila, recognition of diaminopimelic acid-type peptidoglycan by the pattern-recognition receptor PGRP-LE was crucial for the induction of autophagy and that autophagy prevented the intracellular growth of Listeria monocytogenes and promoted host survival after this infection. Autophagy induction occurred independently of the Toll and IMD innate signaling pathways. Our findings define a pathway leading from the intracellular pattern-recognition receptors to the induction of autophagy to host defense.en-USAnimals*AutophagyDiaminopimelic AcidDrosophilaImmunity, InnateListeriaPeptidoglycanToll-Like ReceptorsImmunology and Infectious DiseaseJournal Articlehttps://escholarship.umassmed.edu/infdis_pp/201088917infdis_pp/20