Structural basis for TCR recognition of a Rac1 neoantigen arising from anchor residue mutation.

Abstract excerpt

T cell receptor (TCR)-based immunotherapy can drive cancer regression by targeting neoantigens derived from mutations in self-proteins. Most neoantigens result from mutations in solvent-exposed residues creating neoepitopes that allow highly specific TCR recognition. Here, we describe a melanoma neoantigen (Rac1P29S) caused by a mutation at a primary anchor residue. Unlike typical cases, the immunogenicity of...

Topics

• Humans
• rac1 GTP-Binding Protein
• Mutation
• Receptors, Antigen, T-Cell
• Antigens, Neoplasm
• HLA-A2 Antigen