The DNA Repair Nuclease MRE11A Functions as a Mitochondrial Protector and Prevents T Cell Pyroptosis and Tissue Inflammation (Cell Metabolism)

In rheumatoid arthritis, T cells are deficient in the DNA repair nuclease MRE11A and age prematurely. Li et al. show that MRE11A is necessary to sustain mitochondrial fitness and ATP production. T cells deficient in MRE11A leak mtDNA into the cytoplasm, triggering pyroptosis and driving tissue inflammation.