S. Torres-Odio

Borrelia burgdorferi engages mammalian type I interferon responses via the cGAS-STING pathway

This study shows that Borrelia burgdorferi activates type I interferon responses through the cGAS-STING pathway in mammalian cells.

Activation of the cGAS-STING innate immune response in cells with deficient mitochondrial topoisomerase TOP1MT

This study links TOP1MT deficiency and the P193L variant to mtDNA release and cGAS-STING activation, contributing to autoimmune disease susceptibility.

Type I interferon potentiates metabolic dysfunction, inflammation, and accelerated aging in mtDNA mutator mice

This study shows that type I interferon activation worsens metabolic issues, inflammation, and aging in mice with mitochondrial DNA mutations.

Loss of mitochondrial protease CLPP activates type I interferon responses through the mtDNA-cGAS-STING signaling axis

This study shows that CLPP deficiency causes mtDNA stress, which activates the cGAS-STING pathway and leads to type I interferon responses and antiviral gene expression.

TRIM14 is a key regulator of the type I interferon response during Mycobacterium tuberculosis infection

This study identifies TRIM14 as a negative regulator of the type I interferon response in macrophages during Mycobacterium tuberculosis infection, showing it enhances resolution of the response and limits bacterial replication.

Impaired lysosomal acidification triggers iron deficiency, necrotic cell death and inflammation in vivo

This study shows that impaired lysosomal acidification causes iron deficiency, mitochondrial dysfunction, necrotic cell death, and inflammation in mice.

The splicing factor hnRNP M is a critical regulator of innate immune gene expression in macrophages

This study shows that hnRNP M represses innate immune gene expression in macrophages and its phosphorylation by pathogen sensing cascades regulates splicing to control immune responses.