Protection and compensation in the influenza virus-specific CD8+ T cell response

摘要: Influenza virus-specific CD8+ T cells generally recognize peptides derived from conserved, internal proteins that are not subject to antibody-mediated selection pressure. Prior exposure any one influenza A virus (H1N1) can prime for a secondary cell response serologically different (H3N2). The protection afforded by this recall of established memory, although limited, is negligible. Key characteristics primary and influenza-specific host responses probed here with recombinant viruses expressing modified nucleoprotein (NP) acid polymerase (PA) genes. Point mutations were introduced into the epitopes NP PA such they no longer bound presenting H2Db MHC class I glycoprotein, reassortant H1N1 H3N2 made reverse genetics. Conventional (C57BL/6J, H2b, Ig+/+) Ig-/- (muMT) mice more susceptible challenge single [HKx31 (HK)-NP] (HK-PA) mutants, but unlike mice, Ig+/+ surprisingly resistant HK-NP/-PA double mutant. This was found promote an enhanced IgG resulting, perhaps, delayed elimination antigen-presenting cells. Antigen persistence also could explain increase in size minor KbPB1703 population infected mutant viruses. extent compensation always partial, giving impression operates within constrained limits. It seems relationship between protective humoral cellular immunity neither simple nor readily predicted.