Cell intrinsic immunity spreads to bystander cells via the intercellular transfer of cGAMP

Andrea Ablasser, Jonathan L. Schmid-Burgk, Inga Hemmerling, Gabor L. Horvath, Tobias Schmidt, Eicke Latz and Veit Hornung ()
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Andrea Ablasser: Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn, 53127 Bonn, Germany
Jonathan L. Schmid-Burgk: Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn, 53127 Bonn, Germany
Inga Hemmerling: Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn, 53127 Bonn, Germany
Gabor L. Horvath: Institute of Innate Immunity, University Hospital, University of Bonn, 53127 Bonn, Germany
Tobias Schmidt: Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn, 53127 Bonn, Germany
Eicke Latz: Institute of Innate Immunity, University Hospital, University of Bonn, 53127 Bonn, Germany
Veit Hornung: Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn, 53127 Bonn, Germany

Nature, 2013, vol. 503, issue 7477, 530-534

Abstract: The cytoplasmic DNA receptor cGAS catalyses the synthesis of the second messenger cGAMP, which in turn activates type I interferon via STING; this study shows that cGAMP is transmitted to neighbouring cells via gap junction channels and activates STING, thus inducing an antiviral state in these bystander cells independent of paracrine interferon signalling.

Date: 2013
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DOI: 10.1038/nature12640

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