Du et al. (2025) used a CRISPR-Cas9 gene-edited mouse model to study systemic lupus erythematosus (SLE).
Their research showed that activation of the cGAS-STING pathway is critical in triggering type I interferonopathy, a hallmark of SLE.
Importantly, deleting the cGAS gene in these mice reduced systemic inflammation, indicating that this pathway significantly drives the disease’s inflammatory response.
This study clarifies the molecular basis of SLE’s systemic inflammation and identifies the cGAS-STING pathway as a promising target for treatment.
By inhibiting this pathway, it may be possible to lessen the immune system’s overactivity in SLE, offering new therapeutic possibilities for this complex autoimmune disorder Du et al.
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