NLRC3 puts the brakes on STING

Matthew S J Mangan; Eicke Latz

doi:10.1016/j.immuni.2014.02.007

NLRC3 puts the brakes on STING

Immunity. 2014 Mar 20;40(3):305-6. doi: 10.1016/j.immuni.2014.02.007.

Authors

Matthew S J Mangan¹, Eicke Latz²

Affiliations

¹ Institute of Innate Immunity, University Hospitals, Biomedical Centre, University of Bonn, 53127 Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), 53175 Bonn, Germany.
² Institute of Innate Immunity, University Hospitals, Biomedical Centre, University of Bonn, 53127 Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), 53175 Bonn, Germany; Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01615, USA. Electronic address: [email protected].

Abstract

NOD-like receptors (NLRs) are increasingly implicated in regulating pathogen-sensing pathways. In this issue of Immunity, Zhang et al. (2014) describe a role for NLRC3 in regulating STING and the inflammatory response to cytosolic DNA.

Publication types

Comment

MeSH terms

Animals
DNA / immunology*
Humans
Immunity, Innate*
Intercellular Signaling Peptides and Proteins / genetics*
Intercellular Signaling Peptides and Proteins / metabolism*
Membrane Proteins / metabolism*
Signal Transduction*

Substances

Intercellular Signaling Peptides and Proteins
Membrane Proteins
NLRC3 protein, mouse
Sting1 protein, mouse
DNA

Abstract

Publication types

MeSH terms

Substances

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