Sugar Fix Keeps RIPK3 at Bay

Immunometabolism is emerging as an important modulator of immune responses. In this issue of Immunity, Li et al. (2019) examine the link between lipopolysaccharide (LPS)-induced glucose metabolism and innate immune signaling and identify how β-N-acetylglucosamine (O-GlcNAc) modification of the RIPK3...

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Veröffentlicht in:	Immunity (Cambridge, Mass.) Mass.), 2019-03, Vol.50 (3), p.539-541
Hauptverfasser:	Giogha, Cristina, Lawlor, Kate E.
Format:	Artikel
Sprache:	eng
Schlagworte:	Apoptosis Biosynthesis Cytokines Glucose metabolism Humans Immune response Immune system Immunity Inflammation Kinases Lipopolysaccharides Metabolism N-Acetylglucosamine N-Acetylglucosaminyltransferases Necroptosis Phosphorylation Proteins Receptor-Interacting Protein Serine-Threonine Kinases Rodents Sepsis Serine Sugar Sugars Threonine Tumor necrosis factor-TNF
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Beschreibung
Zusammenfassung:	Immunometabolism is emerging as an important modulator of immune responses. In this issue of Immunity, Li et al. (2019) examine the link between lipopolysaccharide (LPS)-induced glucose metabolism and innate immune signaling and identify how β-N-acetylglucosamine (O-GlcNAc) modification of the RIPK3 RHIM domain limits inflammation and necroptosis. Immunometabolism is emerging as an important modulator of immune responses. In this issue of Immunity, Li et al. (2019) examine the link between lipopolysaccharide (LPS)-induced glucose metabolism and innate immune signaling and identify how β-N-acetylglucosamine (O-GlcNAc) modification of the RIPK3 RHIM domain limits inflammation and necroptosis.
ISSN:	1074-7613 1097-4180
DOI:	10.1016/j.immuni.2019.02.018