ATG16L1 deficiency in macrophages drives clearance of uropathogenic E. coli in an IL-1β-dependent manner

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Lysosomes Integrate Metabolic-Inflammatory Cross-talk in Primary Macrophage Inflammasome Activation

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A Crohn’s disease variant in Atg16l1 enhances its degradation by caspase 3

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Atg16L1 T300A variant decreases selective autophagy resulting in altered cytokine signaling and decreased antibacterial defense

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IL-1 receptor blockade restores autophagy and reduces inflammation in chronic granulomatous disease in mice and in humans

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A Deficiency in the Autophagy Gene Atg16L1 Enhances Resistance to Enteric Bacterial Infection

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The Protein ATG16L1 Suppresses Inflammatory Cytokines Induced by the Intracellular Sensors Nod1 and Nod2 in an Autophagy-Independent Manner

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Selective Subversion of Autophagy Complexes Facilitates Completion of the Brucella Intracellular Cycle

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Defects in autophagy favour adherent-invasive Escherichia coli persistence within macrophages leading to increased pro-inflammatory response

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Sensing and reacting to microbes through the inflammasomes

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Atg16L1 deficiency confers protection from uropathogenic Escherichia coli infection in vivo

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Crohn's disease-associated ATG16L1 polymorphism modulates pro-inflammatory cytokine responses selectively upon activation of NOD2

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Autophagy Suppresses Interleukin-1β (IL-1β) Signaling by Activation of p62 Degradation via Lysosomal and Proteasomal Pathways

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Autophagy Controls IL-1β Secretion by Targeting Pro-IL-1β for Degradation

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Attenuation of human neutrophil migration and function by uropathogenic bacteria

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Non-canonical inflammasome activation targets caspase-11

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Autophagy in immunity and inflammation

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Listeria monocytogenes engineered to activate the Nlrc4 inflammasome are severely attenuated and are poor inducers of protective immunity

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Virus-Plus-Susceptibility Gene Interaction Determines Crohn's Disease Gene Atg16L1 Phenotypes in Intestine

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Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria

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Innate immune detection of the type III secretion apparatus through the NLRC4 inflammasome

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Activation of the Nlrp3 Inflammasome by Streptococcus pyogenes Requires Streptolysin O and NF- B Activation but Proceeds Independently of TLR Signaling and P2X7 Receptor

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Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry

(2009) Leonardo H Travassos et al.   NATURE IMMUNOLOGY

A murine model of urinary tract infection

(2009) Chia-Suei Hung et al.   Nature Protocols

G-CSF induction early in uropathogenicEscherichia coliinfection of the urinary tract modulates host immunity

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A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells

(2008) Ken Cadwell et al.   NATURE

Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production

(2008) Tatsuya Saitoh et al.   NATURE

Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization

(2008) Veit Hornung et al.   NATURE IMMUNOLOGY