Cell-free nucleic acids are released following cell death and inflammation. We have shown that red blood cells (RBCs) express nucleic acid-sensing toll-like receptor 9 (TLR9) and scavenge mitochondrial DNA during homeostasis to prevent lung inflammation. Mitochondrial RNA (mtRNA) is also known as a damage-associated molecular pattern (DAMP) that triggers inflammatory states. Recently, we found that RBCs also express the RNA sensor toll-like receptor 7 (TLR7) on their surface. We hypothesize that RBCs bind and sequester exogenous mtRNA via TLR7, reducing inflammation. This study examines whether RBCs bind mtRNA and if mtRNA activates TLR7. A further understanding of RBCs’ novel role in inflammation could open new avenues to diagnostics and treatments for inflammatory diseases and cancer.