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|Title:||Reversal in the immunodominance hierarchy in secondary CD8+ T cell responses to influenza A virus: roles for cross-presentation and lysis-independent immunodomination.|
|Authors:||Chen, Weisan;Pang, Ken;Masterman, Kelly-Anne;Kennedy, Gina;Basta, Sameh;Dimopoulos, Nektaria;Hornung, Felicita;Smyth, Mark;Bennink, Jack R;Yewdell, Jonathan W|
|Affiliation:||T Cell Laboratory, Ludwig Institute for Cancer Research, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia.|
|Citation:||Journal of Immunology (baltimore, Md. : 1950); 173(8): 5021-7|
|Abstract:||Immunodominance is a central feature of CD8+ T cell (TCD8+) responses to pathogens, transplants, and tumors. Determinants occupy a stable position in an immunodominance hierarchy (alpha-, beta-, etc.) defined by the frequencies of responding TCD8+. In this paper, we study the mechanistic basis for place-swapping between alpha- (acid polymerase (PA)(224-233)) and beta-determinants (nuclear protein 366-374) in primary vs secondary anti-influenza A virus (IAV) responses in mice. This phenomena was recently correlated with the inability of IAV-infected nondendritic cells (DCs) to generate PA(224-233), and it was proposed that secondary TCD8+ are principally activated by IAV-infected epithelial cells, while primary TCD8+ are activated by IAV-infected DCs. In this study, we show that the inability of non-DCs to generate PA(224-232) is relative rather than absolute, and that the preferential use of cross-priming in secondary anti-IAV responses can also account for the revised hierarchy. We further show that immunodomination of PA(224-233)-specific TCD8+ by nucleoprotein 366-374-specific TCD8+ plays a critical role in the phenomena, and that this is unlikely to be mediated by TCD8+ lysis of APCs or other cells.|
|Internal ID Number:||15470045|
Cell Line, Tumor
Influenza A virus.immunology
Mice, Inbred C57BL
|Appears in Collections:||Journal articles|
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