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Deficiency for SAMHD1 activates MDA5 in a cGAS/STING-dependent manner. 2023
Tina Schumann, and
Santiago Costas Ramon, and
Nadja Schubert, and
Mohamad Aref Mayo, and
Melanie Hega, and
Katharina Isabell Maser, and
Servi-Remzi Ada, and
Lukas Sydow, and
Mona Hajikazemi, and
Markus Badstübner, and
Patrick Müller, and
Yan Ge, and
Farhad Shakeri, and
Andreas Buness, and
Benjamin Rupf, and
Stefan Lienenklaus, and
Barbara Utess, and
Lina Muhandes, and
Michael Haase, and
Luise Rupp, and
Marc Schmitz, and
Thomas Gramberg, and
Nicolas Manel, and
Gunther Hartmann, and
Thomas Zillinger, and
Hiroki Kato, and
Stefan Bauer, and
Alexander Gerbaulet, and
Katrin Paeschke, and
Axel Roers, and
Rayk Behrendt
Institute for Immunology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Defects in nucleic acid metabolizing enzymes can lead to spontaneous but selective activation of either cGAS/STING or RIG-like receptor (RLR) signaling, causing type I interferon-driven inflammatory diseases. In these pathophysiological conditions, activation of the DNA sensor cGAS and IFN production are linked to spontaneous DNA damage. Physiological, or tonic, IFN signaling on the other hand is essential to functionally prime nucleic acid sensing pathways. Here, we show that low-level chronic DNA damage in mice lacking the Aicardi-Goutières syndrome gene SAMHD1 reduced tumor-free survival when crossed to a p53-deficient, but not to a DNA mismatch repair-deficient background. Increased DNA damage did not result in higher levels of type I interferon. Instead, we found that the chronic interferon response in SAMHD1-deficient mice was driven by the MDA5/MAVS pathway but required functional priming through the cGAS/STING pathway. Our work positions cGAS/STING upstream of tonic IFN signaling in Samhd1-deficient mice and highlights an important role of the pathway in physiological and pathophysiological innate immune priming.
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