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Significance Many genetic disorders, including Duchenne muscular dystrophy and cystic fibrosis, are caused by a defective protein resulting from a premature termination codon (PTC) in the mutant gene. Aminoglycosides have been proposed as therapies for these disorders because they increase the frequency of translational read-through of PTCs, permitting expression of full-length protein. We consider the possibility that this approach may prompt an autoimmune response to HLA-presented epitopes encoded downstream of the PTC or other stop codons. We demonstrate that gentamicin induces immunologically relevant levels of an epitope derived from PTC read-through. Furthermore, we identify multiple HLA class I-binding peptides derived from read-through of conventional stop codons in gentamicin-treated cells. These results substantiate the possibility of immune autoreactivity from read-through therapies.

Cryptic MHC class I-binding peptides are revealed by aminoglycoside-induced stop codon read-through into the 3′ UTR