作者
Paul Klenerman, Sarah Rowland-Jones, Steve McAdam, Jon Edwards, Susan Daenke, David Lalloo, Britta Köppe, William Rosenberg, Diana Boyd, Anne Edwards, Paul Giangrande, Rodney E Phillips, Andrew J McMichael
发表日期
1994/6/2
期刊
Nature
卷号
369
期号
6479
页码范围
403-407
出版商
Nature Publishing Group UK
简介
MOST asymptomatic individuals infected with HIV-1 have a cyto-toxic T lymphocyte (CTL) response to the virus Gag proteins which can be demonstrated in vitro1,2. Epitopes have been mapped in p17 Gag and p24 Gag restricted by HLA-B8 (p17-3 and p24-13) and -B27 (p24-14) 2,3. Viruses isolated from patients who make CTL responses to these peptides vary within the genetic sequences encoding these epitopes and some mutations lead to reduction in killing activity in vitro4. This was attributed to either failure of the variant epitope to bind major histocompatibility complex class I or failure of T-cell receptors to bind the presented peptide. But peptide variants of class I-restricted epitopes cause 'antagonism', that is, the presence of a variant epitope (in the form of peptide) inhibits normal lysis of targets presenting the original epitope5,6. This mirrors similar findings in class II-restricted systems7–10. Here we report …
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P Klenerman, S Rowland-Jones, S McAdam… - Nature, 1994