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ERADication of STING limits inflammation

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The cGAS–STING cytosolic double-stranded-DNA-sensing pathway provides protection against infection but also contributes to inflammatory pathology and thus must be tightly regulated. In this issue, Jie et al. find that endoplasmic-reticulum-associated degradation of the adaptor STING by SEL1L–HRD1 controls steady-state STING levels to limit STING-driven inflammation.

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Fig. 1: The pool of resting STING at the ER is limited by SEL1L–HRD1-mediated ERAD.

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Authors and Affiliations

  1. University of Massachusetts Chan Medical School of Medicine, Worcester, MA, USA

    Kevin MingJie Gao & Katherine A. Fitzgerald

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  1. Kevin MingJie Gao
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  2. Katherine A. Fitzgerald
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Correspondence to Katherine A. Fitzgerald.

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Competing interests

K.F. is a scientific founder of Danger Bio, a Related Sciences company, and is a member of the scientific advisory board for Vesigen Therapeutics, NodThera, Janssen and Generation Bio. K.M.G. declares no competing interests.

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Gao, K.M., Fitzgerald, K.A. ERADication of STING limits inflammation. Nat Cell Biol 25, 635–636 (2023). https://doi.org/10.1038/s41556-023-01142-8

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