tRNA derived fragment (tRF)-3009 participates in modulation of IFN-α-induced CD4+ T cell oxidative phosphorylation in lupus patients

Abstract Background Accumulating evidence suggests tRNA-derived fragments (tRFs) play important roles in cellular homeostasis. Here we aimed to explore aberrant expression of tRFs CD4 + T cells from patients with systemic lupus erythematosus (SLE) and their potential function the SLE pathogenesis. Methods First, small RNA sequencing was performed on four three healthy controls (HCs). Candidate were then validated 97 relevant disease using qRT-PCR. Then used investigate profiles HC-derived transfected tRF-3009 . Lastly, siRNA or mimics into with/without IFN-α. Changes oxygen consumption rate (OCR), ATP, ROS production analyzed. Results We identified 482 differentially expressed chose for further analysis due its upregulation positive correlations between SLEDAI, active nephritis serum IFN-α levels. In vitro, over-expressing cell profiling putative linked this product type I IFN oxidative phosphorylation (OXPHOS) pathways. Interestingly, is capable inducing ATP cells, while knockdown reversed process. Overexpression alone sufficient upregulate OCR, ROS, production. Conclusions Our study first link tRF SLE. may participate metabolic modulation IFN-α-induced OXPHOS lupus.