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¹ Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, OX3 9DS, UK
² Division of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK
³ Department of HIV/GUM, The Guy's, Kings' and St Thomas' School of Medicine, Weston Education Centre, London, SE5 9RS, UK
⁴ Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, OX3 9DU, UK
⁵ Sir William Dunn School of Pathology, Oxford University, Oxford, OX1 3RE,UK
⁶ San Diego VA Research Center for AIDS and HIV Infection, University of California San Diego, La Jolla, CA 92093

Address correspondence to Sarah L. Rowland-Jones, MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS UK. Phone: 44-1865-222316; Fax: 44-1865-222502; email: sarah.rowland-jones{at}ndm.ox.ac.uk

HIV-specific cytotoxic T lymphocytes (CTL) are important in controlling HIV replication, but the magnitude of the CTL response does not predict clinical outcome. In four donors with delayed disease progression we identified Vß13.2 T cell receptors (TCRs) with very similar and unusually long ß-chain complementarity determining region 3 (CDR3) regions in CTL specific for the immunodominant human histocompatibility leukocyte antigens (HLA)-B8–restricted human immunodeficiency virus-1 (HIV-1) nef epitope, FLKEKGGL (FL8). CTL expressing Vß13.2 TCRs tolerate naturally arising viral variants in the FL8 epitope that escape recognition by other CTL. In addition, they expand efficiently in vitro and are resistant to apoptosis, in contrast to FL8–specific CTL using other TCRs. Selection of Vß13.2 TCRs by some patients early in the FL8-specific CTL response may be linked with better clinical outcome.

Key Words: HIV • cytotoxic T lymphocytes (CTL) • T cell receptor • cross-reactivity • apoptosis

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