The strength and quality of TCR signaling, which is determined by the affinity of the TCR for peptide–MHC molecules (pMHC), the dose of antigen presented by APCs, the duration of the TCR–pMHC interaction, and the timing of TCR recognition (early or late during infection phase) have been shown to partially contribute to memory commitment, function and the diversity of the memory pool (48). This evidence concerns the gene HLA-C and infection.