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Ladell, Kristin; Hashimoto, Masao; Iglesias, Maria Candela; Wilmann, Pascal G.; McLaren, James E.; Gras, Stéphanie; Chikata, Takayuki; Kuse, Nozomi; Fastenackels, Solène; Gostick, Emma; Bridgeman, John S.; Venturi, Vanessa; Arkoub, Zaïna Aït; Agut, Henri; van Bockel, David J.; Almeida, Jorge R.; Douek, Daniel C.; Meyer, Laurence; Venet, Alain; Takiguchi, Masafumi; Rossjohn, Jamie; Price, David A.; Appay, Victor
Immunity, 03/2013, Letnik: 38, Številka: 3Journal Article
The capacity of the immune system to adapt to rapidly evolving viruses is a primary feature of effective immunity, yet its molecular basis is unclear. Here, we investigated protective HIV-1-specific CD8+ T cell responses directed against the immunodominant p24 Gag-derived epitope KK10 (KRWIILGLNK263-272) presented by human leukocyte antigen (HLA)-B∗2705. We found that cross-reactive CD8+ T cell clonotypes were mobilized to counter the rapid emergence of HIV-1 variants that can directly affect T cell receptor (TCR) recognition. These newly recruited clonotypes expressed TCRs that engaged wild-type and mutant KK10 antigens with similar affinities and almost identical docking modes, thereby accounting for their antiviral efficacy in HLA-B∗2705+ individuals. A protective CD8+ T cell repertoire therefore encompasses the capacity to control TCR-accessible mutations, ultimately driving the development of more complex viral escape variants that disrupt antigen presentation. ► New T cell clonotypes are recruited to counter TCR-accessible HIV mutations ► These T cells express TCRs that crossrecognize wild-type and mutant epitopes ► Crossreactive CD8+ T cells underpin anti-HIV efficacy in HLA-B∗27+ patients ► T cell efficacy ultimately drives escape mutations that impact antigen presentation
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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