Schlafen 11 triggers innate immune responses through its ribonuclease activity upon detection of single-stranded DNA.
Peng ZhangXiaoqing HuZe-Kun LiQian LiuLele LiuYing-Ying JinSizhe LiuXiang ZhaoJianqiao WangDelong HaoHou-Zao ChenDe-Pei LiuPublished in: Science immunology (2024)
Nucleic acids are major structures detected by the innate immune system. Although intracellular single-stranded DNA (ssDNA) accumulates during pathogen infection or disease, it remains unclear whether and how intracellular ssDNA stimulates the innate immune system. Here, we report that intracellular ssDNA triggers cytokine expression and cell death in a CGT motif-dependent manner. We identified Schlafen 11 (SLFN11) as an ssDNA-activated RNase, which is essential for the innate immune responses induced by intracellular ssDNA and adeno-associated virus infection. We found that SLFN11 directly binds ssDNA containing CGT motifs through its carboxyl-terminal domain, translocates to the cytoplasm upon ssDNA recognition, and triggers innate immune responses through its amino-terminal ribonuclease activity that cleaves transfer RNA (tRNA). Mice deficient in Slfn9, a mouse homolog of SLFN11, exhibited resistance to CGT ssDNA-induced inflammation, acute hepatitis, and septic shock. This study identifies CGT ssDNA and SLFN11/9 as a class of immunostimulatory nucleic acids and pattern recognition receptors, respectively, and conceptually couples DNA immune sensing to controlled RNase activation and tRNA cleavage.
Keyphrases
- immune response
- dendritic cells
- cell death
- toll like receptor
- circulating tumor
- single molecule
- nucleic acid
- cell free
- septic shock
- poor prognosis
- binding protein
- type diabetes
- oxidative stress
- dna methylation
- drug induced
- genome wide
- metabolic syndrome
- hepatitis b virus
- candida albicans
- mass spectrometry
- extracorporeal membrane oxygenation
- acute respiratory distress syndrome
- endothelial cells
- cell cycle arrest
- long non coding rna
- wild type